BIOLOGY ASSIGNMENT
BIOLOGY ASSIGNMENTNEURONAL ANTI-AGING PROPOSAL
BIOLOGY ASSIGNMENTNEURONAL ANTI-AGING PROPOSAL
Bryan Anthony Bruyns1300810Liew Jia Ying1300651Prasana A/P
Rasiah1300878Sivasshnee A/P Maniam1200563Sylvia Chong Syin
Ying1300748Terence Chin1300635
CONTENTNo.TopicPage1.0IntroductionNeuronNeuron Structures and
FunctionsEffect of NeurodegenerationStem Cell Anti-Aging and
RejuvenationThe Basic of Recombinant rDNAMethods of Making
Recombinant rDNAFunctions of rDNAImportance of Recombinant
DNAMotivationJustification4-8910-1112-1718-212223-24252627282.0
Objective2.1 Objective of Invention of Anti-Aging Medicine2.2 To
Extract DNA from Human 2.3 Exchange in Genetic Materials2.4 To
Produce a New Recombinant DNA2.5 Human Anti-Aging Gene2.6
Anti-Aging Firewalls2.7 The Ways to Solve Problems
Faced293031-33343536-38393.0MethodsSkin Cell as A Source of
NeuronsTreatments and Cure4041No.TopicPage4.0Expected
Results425.0Reference43
IntroductionAging of the nervous system underlies the behavioral
and cognitive decline associated with senescence. Understanding the
molecular and cellular basis of neuronal aging will therefore
contribute to the development of effective treatments for aging and
age-associated neurodegenerative disorders. Despite this pressing
need, there are surprisingly few animal models that aim at
recapitulating neuronal aging in a physiological context. We
recently developed a C. elegans model of neuronal aging, and showed
that insulin signaling regulates age-dependent neuronal defects. We
identified electrical activity and epithelial attachment as two
critical factors in the maintenance of structural integrity of C.
elegans touch receptor neuron. These findings open a new avenue for
elucidating the molecular mechanisms that maintain neuronal
structures during the course of aging Our recent Caenorhabditis
elegans model of neuronal aging presents two important features
that distinguish it from previous vertebrate models of
neurodegenerative diseases. First, through the first longitudinal
imaging of single neurons across the entire adult lifespan, our
model reveals unexpected dynamic features of neuronal aging that
are not adequately appreciated in existing animal models of brain
aging. Second, our model had identified factors that are
specifically required for neuronal integrity without affecting
organismal lifespan, indicating that lifespan and cellular aging
could be mechanistically uncoupled.
Dynamic Features of Neuronal agingFor most metazoan, including
C. elegans aging of the nervous system is not associated with
significant neuronal loss. At the cellular level, the cardinal
features of an aging human brain include dystrophic neurites,
neurofibrillary tangles and insoluble protein aggregates. How these
cellular defects evolve over time is still a mystery. Life-long
tracking of individual aging neurons is difficult in lab mammals,
however, due to their relatively long lifespan and the
extraordinarily huge number of neurons in the mammalian brain. In
contrast to previous reports that found no evidence for neuronal
aging in C. elegans, we documented various types of age-dependent
defects in C. elegans touch receptor and motor neurons, including
misshapen neuronal soma, aberrant neurite information, and beading
or bubble-like lesions in the nerve processes. Similar to our
findings, Tank et al. had recently reported age-dependent neurite
sprouting in C. elegans. One striking feature revealed by our
longitudinal imaging in touch neurons is the frequent growth and
retraction of abnormal neuritis. Age-dependent loss of dendritic
branches had been found in mammalian neurons. By contrast,
generation of new neurites in middle and late life of a neuron had
never been documented. It is unclear whether there neurites form
synaptic connections with other neurons, although they contain
acetylated microtubules. The emergence of there neurites may
represent a failure of the aged neuron to suppress unwanted growth
rather than an enhanced ability to generate new structures, judging
from their short length , random growth patterns and frequent
retraction. Tank et al. had shown that activity of the Jun kinase
pathway is required to suppress there age-dependent neuronal
sprouting, Since rescued jnk-1 mutant animals overexpressing the C.
elegens c-jun N-terminal kinase JNK-1 still show neuronal sprouting
comparable to that in age-matched wild type, age-dependent loss of
JNK-1 activity cannot be the sole explanation for senescent
neuronal sprouting in C. elegans. It will be of interest to test
whether aberrant neurite outgrowth is regulated by cytoskeletal
machinery that also controls developmental axon extension, and what
additional mechanisms normally keep their aberrant outgrowth in
check. Another prominent age-dependent defect of C. elegans touch
neuron process in beading or bubble-like lesions, and our
longitudinal imaging suggests that some of the minor beading my
represent bubble-like lesions in their early phase. Axon beading is
common is neurons subjected to traumatic, hypoxic or inflammatory
insults. In these conditions, beading may represent cytoskeletal
defects or focal accumulation of axoplasmic cargos or organelles
due to disrupted axonal transport. Identity of ge-dependent axon
beading remains obscure in both human and C. elegans.
Interestingly, in some neurons at extremely old age, we observed
axon splitting. Because multiple bubbles like lesions could be
found to coexist on the same axon, a wild speculation is that some
of the bubble-like lesions are early focal splitting of the axon.
Electron microscopy will be necessary to clarify the nature of
their age-dependent axonal defects in C. elegans neurons.
Neuron-Specific Anti-Aging MechanismsThe stochastic feature of
aging describes that in individual animals, the physiological age
does not necessarily correlate with its chronological age. Thus,
neurons from mid-age C. elegans may have extensive defects, whereas
neurons from an animal at advanced age may appear intact. On the
other hand, individual tissues show great variations in the rate of
aging. However, it is still believed that tissue aging worsens as
the chronological age advances and the regulation of lifespan and
cellular aging is tightly linked. We and Tank et al. had identified
electrical activities, nerve attachment, JNK and insulin signaling
as potentially autonomous factors that contribute to neuronal
integrity during aging. Surprisingly, in both studies neuronal
aging could be uncoupled from organismal aging. Mutations in mec-1
ad mec-12, which encode an ECM protein and -tubulin, respectively,
accelerate neuronal aging without affecting lifespan. Similarly,
disrupting JNK signaling aggravates age-dependent neurite sprouting
but does not decrease lifespan. These observations indicate that at
the cellular level, aging is regulated in a tissue-specific manner,
and is not necessarily linked to lifespan regulation.Electrical
activity had been shown to be essential for adult Drosophila
olfactory neurons to survive and for newly generated hippocampal
neurons to integrate into the adult neural circuits. Our study
extends the roles of electrical activity in the maintenance of
adult nervous system, and raises several issues that await
exploration in the near future. First, does physiological membrane
activity constantly activate signaling pathways that promote
neuronal integrity, or does it act to sup- press cellular machinery
that dismantles the neurons? These two possibilities are not
mutually exclusive and may cooperate to achieve optimal neuronal
maintenance against aging.Second, what is the signaling pathway
that translates electrical activity on the plasma membrane into
transcriptional and posttranslational mechanisms for neuronal
maintenance? Calcium emerges as a promising target, in that its
wide spectrum of intracellular dynamics makes it one of the most
versatile second messengers in cellular physiology. Previous
studies indicate that aged hippocampal neurons show more pronounced
increase in intracellular calcium level under stimulation, compared
with young neurons. Deranged regulation of intracellular calcium
may underlie some of the functional decline seen in the aged
neurons. In larval C. elegans, calcium had been shown to mediate
necrotic neuronal death induced by excessive sodium channel
activity. On the other hand, regeneration of touch neuron processes
after laser axotomy requires calcium. Whether calcium promotes
regenerative behaviors of injured neurons or causes the neuron to
die may depend on its temporal dynamics. Rapid, massive calcium
increase in the cytosol may activate proteolytic enzymes that
dismantle the neuron, whereas persistent, low-grade calcium flow
could activate cellular pathways that contribute to axon repair or
neuronal integrity for a long run. One of the future challenges
will be to monitor neuronal calcium dynamics in an extended
temporal dimension that is relevant to aging.In conclusion, the C.
elegans model of neuronal aging reveals novel age-dependent defects
that are highly dynamic, and had identified several factors
specifically required for the maintenance of neuronal integrity
during aging. It is important to verify these observations in other
organisms such as Drosophila, mouse or human. A future goal will be
to unravel the genetic control of age-dependent neuronal defects
through forward and reverse genetics approaches.
1.1 Neuron
A neuron is an electrically excitable cell that processes and
transmits information through electrical and chemical signals.
These signals between neurons occur via synapses, specialized
connections with other cells. Neurons can connect to each other to
form neural networks. Neurons are the core components of the
nervous system, which includes the brain, and spinal cord of the
central nervous system (CNS), and the ganglia of the peripheral
nervous system (PNS). A typical neuron possesses a cell body,
dendrites, and an axon. The term neurite is used to describe either
a dendrite or an axon, particularly in its undifferentiated stage.
Dendrites are thin structures that arise from the cell body, often
extending for hundreds of micrometres and branching multiple times,
giving rise to a complex "dendritic tree". An axon is a special
cellular extension that arises from the cell body at a site called
the axon hillock and travels for a distance, as far as 1 meter in
humans or even more in other species. The cell body of a neuron
frequently gives rise to multiple dendrites, but never to more than
one axon, although the axon may branch hundreds of times before it
terminates. At the majority of synapses, signals are sent from the
axon of one neuron to a dendrite of another. There are, however,
many exceptions to these rules: neurons that lack dendrites,
neurons that have no axon, and synapses that connect an axon to
another axon or a dendrite to another dendrite.All neurons are
electrically excitable, maintaining voltage gradients across their
membranes by means of metabolically driven ion pumps, which combine
with ion channels embedded in the membrane to generate
intracellular-versus-extracellular concentration differences of
ions such as sodium, potassium, chloride, and calcium. Changes in
the cross-membrane voltage can alter the function of
voltage-dependent ion channels. If the voltage changes by a large
enough amounts, an all-or-none electrochemical pulse called an
action potential is generated, which travels rapidly along the
cell's axon, and activates synaptic connections with other cells
when it arrives.The more neurons (millions) activated into
synchronous cell assemblies, the greater your cognitive power.
1.1.1 Neuron Structures and Functions:
Sensory NeuronThe stimulus is a change in the internal or
external environment
InterneuronThe stimulus is a neurotransmitter (chemical)
released from a sensory neuron or another interneuron. Found in
brain and spinal cord.
Motor neuronThe stimulus is a neurotransmitter released from an
interneuron. These neurons send messages to muscles or glands.
*Glands need a message from the (word) before they can carry out
their function.
DendritesNeuron parts that detect the stimulus
Cell bodyNeuron part that contains most of the cytoplasm and the
nucleus.
SynapseSpace between two neurons or between a neuron and an
effector. This is where neurotransmitters get released.
AxonNeuron part that sends an action potential(nerve impulse)
away from the cell body
Axon EndingsEnds of axons that contain vesicles with NTs
(neurotransmitter)
Myelin SheathLayer of lipid rich (fatty rich) cells wrapped
around the axon to prevent electrolyte (Na+, K+) loss
EffectorA muscle or a gland (respond to stimulus) that receives
a message from a motor neuron
Nodes of RanvierGaps in myelin
DendritesShort branches of a neuron that receives stimuli and
conduct impulses to the cell body.
Cell BodyThe center of metabolic activity in a neuron, it is
where the nucleus and much of the cytoplasm are located.
AxonThe long fiber that carries impulses away from the cell
body
Sensory NeuronsCarry impulses from outside and inside the body
to the brain and spinal cord
Motor NeuronsCarry response impulses from the brain and spinal
cord to muscles or glands
InterneuronsConnect sensory neurons and motor neurons and carry
impulses between them. They are concentrated in the brain and
spinal cord.
1.1.2 Effect of NeurodegenerationNeurodegeneration is the
umbrella term for the progressive loss of structure or function of
neurons, including death of neurons. Many neurodegenerative
diseases including Parkinsons, Alzheimers, and Huntingtons occur as
a result of neurodegenerative processes. As research progresses,
many similarities appear which relate these diseases to one another
on a sub-cellular level. Discovering these similarities offers hope
for therapeutic advances that could ameliorate many diseases
simultaneously. There are many parallels between different
neurodegenerative disorders including atypical protein assemblies
as well as induced cell death. Neurodegeneration can be found in
many different levels of neuronal circuitry ranging from molecular
to systemic.Alzheimer DiseaseAlzheimer's disease is characterized
by loss of neurons and synapses in the cerebral cortex and certain
subcortical regions. This loss results in gross atrophy of the
affected regions, including degeneration in the temporal lobe and
parietal lobe, and parts of the frontal cortex and cingulate
gyrusAlzheimer's disease has been hypothesized to be a protein
misfolding disease (proteopathy), caused by accumulation of
abnormally folded A-beta and tau proteins in the brain. Plaques are
made up of small peptides, 3943amino acids in length, called
beta-amyloid (also written as A-beta or A). Beta-amyloid is a
fragment from a larger protein called amyloid precursor protein
(APP), a transmembrane protein that penetrates through the neuron's
membrane. APP is critical to neuron growth, survival and
post-injury repair. In Alzheimer's disease, an unknown process
causes APP to be divided into smaller fragments by enzymes through
proteolysis. One of these fragments gives rise to fibrils of
beta-amyloid, which form clumps that deposit outside neurons in
dense formations known as senile plaques.
Parkinson DiseaseParkinson's disease is the second most common
neurodegenerative disorder and manifests as bradykinesia, rigidity,
resting tremor and posture instability. The crude prevalence rate
of PD has been reported to range from 15 per 100,000 to 12,500 per
100,000, and the incidence of PD from 15 per 100,000 to 328 per
100,000, with the disease being less common in Asian countries.
Parkinson's disease is a degenerative disorder of the central
nervous system. It results from the death of dopamine-generating
cells in the substantia nigra, a region of the midbrain; the cause
of cell-death is unknown. The following paragraph is an excerpt
from the Pathophysiology section of the article Parkinson's
disease.The mechanism by which the brain cells in Parkinson's are
lost may consist of an abnormal accumulation of the protein
alpha-synuclein bound to ubiquitin in the damaged cells. The
alpha-synuclein-ubiquitin complex cannot be directed to the
proteosome. This protein accumulation forms proteinaceous
cytoplasmic inclusions called Lewy bodies. The latest research on
pathogenesis of disease has shown that the death of dopaminergic
neurons by alpha-synuclein is due to a defect in the machinery that
transports proteins between two major cellular organelles the
endoplasmic reticulum (ER) and the Golgi apparatus. Certain
proteins like Rab1 may reverse this defect caused by
alpha-synuclein in animal models.Recent research suggests that
impaired axonal transport of alpha-synuclein leads to its
accumulation in the Lewy bodies. Experiments have revealed reduced
transport rates of both wild-type and two familial Parkinson's
disease-associated mutant alpha-synucleins through axons of
cultured neurons. Membrane damage by alpha-synuclein could be
another Parkinson's disease mechanism. The main known risk factor
is age. Susceptibility genes including -synuclein, leucine rich
repeat kinase 2 (LRRK-2), and glucocerebrosidase (GBA) have shown
that genetic predisposition is another important causal factor.
Huntingtons DiseaseThe following paragraph is an excerpt from
the Mechanism section of the article Huntington's
disease.Huntingtons disease causes astrogliosis and loss of medium
spiny neurons. Areas of the brain are affected according to their
structure and the types of neurons they contain, reducing in size
as they cumulatively lose cells. The areas affected are mainly in
the striatum, but also the frontal and temporal cortices. The
striatum's subthalamic nuclei send control signals to the globus
pallidus, which initiates and modulates motion. The weaker signals
from subthalamic nuclei thus cause reduced initiation and
modulation of movement, resulting in the characteristic movements
of the disorder.Mutant Huntingtin is an aggregate-prone protein.
During the cells' natural clearance process, these proteins are
retrogradely transported to the cell body for destruction by
lysosomes. It is a possibility that these mutant protein aggregates
damage the retrograde transport of important cargoes such as BDNF
by damaging molecular motors as well as microtubules.Amyotrophic
lateral sclerosis Amyotrophic lateral sclerosis (ALS/Lou Gehrigs
Disease) is a disease in which motor neurons are selectively
targeted for degeneration. In 1993, missense mutations in the gene
encoding the antioxidant enzyme Cu/Zn superoxide dismutase 1 (SOD1)
were discovered in subsets of patients with familial ALS. This
discovery led researchers to focus on unlocking the mechanisms for
SOD1-mediated diseases. Unfortunately, the pathogenic mechanism
underlying SOD1 mutant toxicity has yet to be resolved. More
recently, TDP-43 and FUS protein aggregates have been implicated in
some cases of the disease, and a mutation in chromosome 9 (C9orf72)
is thought to be the most common known cause of sporadic ALS.Recent
independent research by Nagai et al. and Di Giorgio et al.provide
in vitro evidence that the primary cellular sites where SOD1
mutations act are located on astrocytes. Astrocytes then cause the
toxic effects on the motor neurons. The specific mechanism of
toxicity still needs to be investigated, but the findings are
significant because they implicate cells other than neuron cells in
neurodegeneration.Aging and neurodegenerationThe greatest risk
factor for neurodegenerative diseases is aging. Mitochondrial DNA
mutations as well as oxidative stress both contribute to aging.
Many of these diseases are late-onset, meaning there is some factor
that changes as a person ages for each disease. One constant factor
is that in each disease, neurons gradually lose function as the
disease progresses with age.TherapeuticsThe process of
neurodegeneration is not well understood so the diseases that stem
from it have, as yet, no cures. In the search for effective
treatments (as opposed to palliative care), investigators employ
animal models of disease to test potential therapeutic agents.
Model organisms provide an inexpensive and relatively quick means
to perform two main functions: target identification and target
validation. Together, these help show the value of any specific
therapeutic strategies and drugs when attempting to ameliorate
disease severity. An example is the drug Dimebon (Medivation). This
drug is in phase III clinical trials for use in Alzheimers disease,
and also recently finished phase II clinical trials for use in
Huntingtons disease.In another experiment using a rat model of
Alzheimer's disease, it was demonstrated that systemic
administration of hypothalamic proline-rich peptide (PRP)-1 offers
neuroprotective effects and can prevent neurodegeneration in
hippocampus amyloid-beta 2535. This suggests that there could be
therapeutic value to PRP-1.Protein degradation offers therapeutic
options both in preventing the synthesis and degradation of
irregular proteins. There is also interest in upregulating
autophagy to help clear protein aggregates implicated in
neurodegeneration. Both of these options involve very complex
pathways that we are only beginning to understand.The goal of
immunotherapy is to enhance aspects of the immune system. Both
active and passive vaccinations have been proposed for Alzheimer's
disease and other conditions, however more research must be done to
prove safety and efficacy in humans.Anti-AgingAnti-aging medicine
is a clinical specialty is founded on the application of advanced
scientific and medical technologies for the early detection,
prevention, treatment, and reversal of age-related dysfunction,
disorders, and diseases. It is a healthcare model promoting
innovative science and research to prolong the healthy lifespan in
humans. As such, anti-aging medicine is based on principles of
sound and responsible medical care that are consistent with those
applied in other preventive health specialties. The phrase
"anti-aging," as such, relates to the application of advanced
biomedical technologies focused on the early detection, prevention,
and treatment of aging-related disease. Anti-aging medicine
complements regenerative medicine, as both specialties embrace
cutting-edge biomedical technologies aimed at achieving benefits
for both the quality and quantity of the human lifespan. Some of
the most promising aspects of regenerative medicine, most notably:
Stem cell therapeutics, technologies aiming to beneficially alter
the very basic cellular sources of dysfunctions, disorders,
disabilities, and diseases Therapeutic cloning, technologies to
develop ample sources of human cells, tissues, and organs for use
in acute emergency care as well as the treatment of chronic,
debilitating diseases Genetic engineering and genomics,
advancements that permit the identification and alteration of
genetics to ameliorate dysfunctions, disorders, disabilities, and
diseases Nanotechnology, deploying micro- and molecular-sized tools
to manipulate human tissue biology for microsurgical repair on a
gross level, as well as microscopic nano-biology for repair at the
most basic cellular levelTaken collectively, the advancements
offered by anti-aging and regenerative medicine to improve the
quality of, and/or extend the length of, the human lifespan, are
the singlemost potent emerging biomedical technologies
today.Universally, those involved in healthcare, or those whose
fields of expertise intersect with healthcare issues, support
anti-aging medicine as a healthcare model promoting innovative
science and research to prolong the healthy human lifespan. Public
policy organizations and government agencies in a number of nations
are now embracing anti-aging medicine as a viable solution to
alleviate the mounting social, economic, and medical woes otherwise
anticipated to arrive with the trend of unprecedented global aging.
Anti-aging medicine is now practiced by thousands of physicians in
private medical offices, as well as at some of the most prestigious
teaching hospitals around the world. Involving a patient base in
the hundreds of thousands worldwide, anti-aging medicine is
achieving demonstrable and objective results that beneficially
impact the degenerative diseases of aging.1.1.3 Stem Cell
Anti-Aging and Rejuvenation
How Stem Cells Prevent Aging:Aging results from the progressive
depletion of stem cells, so the introduction of new stem cells has
the potential of slowing down or reversing this process."Stem cell
therapies are among the world's greatest collective scientific
breakthrough, possessing the clear potential to revolutionize the
practice of medicine and improve the quality and length of life."
Townsend Letter for Doctors and Patients.Stem cells possess a
unique anti-aging effect by improving immune function and
regenerating and repairing organs damaged by stressors, like free
radicals and the various toxins we are exposed to in our day to day
living.
How Stem Cells Prevent Aging:Your body uses its own stem cells
to make you stronger, healthier and more resistant to disease. As
we age, we use stem cells to repair damaged organs, or to replace
those stem cells destroyed by toxins over time.At all stages of
your life, your body fights damage by using stem cells. When you
smoke, stem cells head for the lungs. When you are sun burnt, they
repair the skin. As late as the early 2000's, we did not know that
stem cell replenishment was true for most organs, but today we know
that every organ seems to recruit stem cells from the bone marrow
to resuscitate itself.
Decline in stem cell production with age:Decline in stem cell
production with age As we age, however, the bone marrow releases
fewer stem cells, giving us less power to repair the damage of
ageing. Treatment with adult stem cells reverses this process.In
healthy individuals, skin youthfulness is maintained by epidermal
stem cells which self-renew and generate daughter cells that become
new skin. Despite accumulation of aging blemishes and changes in
aged skin, epidermal stem cells are maintained at normal levels
throughout life. Therefore, skin ageing is caused by impaired stem
cell mobilization from the bone marrow or reduced number of stem
cells able to respond to repair signals. (6). This means that, if
we increase the number of circulating stem cells, by mobilizing
from the bone marrow, and by infusion of additional stem cells we
should dramatically change this cell behavior.It has been
postulated that stem cell exhaustion from the bone marrow is partly
responsible for the process of cardiovascular ageing and the
resulting diseases such as angina, heart attack, stroke and senile
dementia. It has now been proven that stem cell damage in the bone
marrow, from aging, is responsible for coronary artery disease and
resultant cardiac muscle damage. This means that cardiac disease
can be prevented by stem cell therapy.
Decline in stem cell production with age:As aging progresses,
there is a decline in the brain's capacity to produce new neurons.
The underlying cause of the declining neurogenesis is unknown, but
is presumably related to age-related changes that occur during
normal aging of the brain. It is exacerbated by age-related
neurodegenerative diseases such as Alzheimer's and Parkinson's
diseases.
The most powerful solution:According to the American Academy of
Anti-aging Medicine, stem cells appear to be our most powerful tool
in Regenerative Medicine at this time. Previous dogma concerning
adult stem cells taught that our tissues did not have stem cells
and the cells present at birth just declined in quantity and
quality until there was nothing left. It was also believed that
hematopoietic stem cells lacked plasticity and could not transform
to other tissues.Current medical literature proves that adult stem
cells exist in most tissues including brain, heart, muscles and
liver and adult stem cells have plasticity to potentially transform
and repair all tissues and organs.Current literature also shows
that stem cell supplementation of an age-damaged bone marrow stem
cell population can result in rejuvenation and the increase in
longevity of that stem cell source.
Specific age-related conditions can be treated:Osteoarthritis
responds well to joint infusions of stem cells as shown in phase
III trials in the USA. Early Alzheimers disease can be reversed and
Parkinsons disease has shown excellent improvement when treated in
the early stages. Emotional and cognitive improvement occurs, which
you will notice as your memory improves, concentration ability
increases and your ability to handle complex tasks, as you did
before, is regained. An increase in energy levels and a resistance
to disease develops as your cardiovascular, nervous and immune
systems are boosted by the stem cell infusion. You will find that
you will have higher levels of energy than before.
The Beauty Response from Stem CellsThe most evident beauty
response in stem cell treated patients is the appearance of the
facial skin a few weeks after therapy - it glows. You will notice a
smoothness and improvement in color along with a look of
youthfulness.Grey hair has been noted to regain its original color
and bald spots have filled in. The rest of your skin will show an
improvement in color and age-related pigmentation marks, less
bruising and an increase in elasticity and tone.
Overall improvements:You can expect improvements after stem cell
therapy, including but not limited to:1. Physical improvements such
as: Less head/neck aches Decreased soreness in neck, arms and legs
Reduced stiffness in joints Far less tiredness or fatigue2.
Aesthetic improvements such as: The skin on the face and hands
becomes tighter Fewer wrinkles Looking younger - general younger
appearance Change in color of hair from grey to black/normal Hair
thickens3. Mental and Emotional improvements.4. Improvements in
Energy Levels.5. Improvement in the Overall Quality of Life.
Life extension science, also known as anti-aging medicine,
indefinite life extension, experimental gerontology, and biomedical
gerontology, is the study of slowing down or reversing the
processes of aging to extend both the maximum and average lifespan.
Some researchers in this area, and "life extensionists",
"immortalists" or "longevists" (those who wish to achieve longer
lives themselves), believe that future breakthroughs in tissue
rejuvenation with stem cells, molecular repair, and organ
replacement (such as with artificial organs or
xenotransplantations) will eventually enable humans to have
indefinite lifespans (agerasia) through complete rejuvenation to a
healthy youthful condition.The sale of putative anti-aging products
such as nutrition, physical fitness, skin care, hormone
replacements, vitamins, supplements and herbs is a lucrative global
industry, with the US market generating about $50 billion of
revenue each year. Some medical experts state that the use of such
products has not been proven to affect the aging process, and many
claims of anti-aging medicine advocates have been roundly
criticized by medical experts, including the American Medical
Association.However, it has not been shown that the goal of
indefinite human lifespans itself is necessarily unfeasible; some
animals such as lobsters and certain jellyfish do not die of old
age, and an award was offered to anyone who could prove life
extensionist Aubrey de Grey's hopes were 'unworthy of learned
debate'; the challenge remains open. The ethical ramifications of
life extension are debated by bioethicists.
1.2 The Basic of Recombinant rDNA
Recombinant DNA (DNA) molecules are DNA molecules formed by
laboratory methods of genetic recombination (such as molecular
cloning) to bring together genetic material from multiple sources,
creating sequences that would not otherwise be found in biological
organisms. Recombinant DNA is possible because DNA molecules from
all organisms share the same chemical structure. They differ only
in the nucleotides sequence within that identical overall
structure.Recombinant DNA molecules are sometimes called chimeric
DNA, because they are usually made of material from two different
species, like the mythical chimera. R-DNA technology uses
palindromic sequences and leads to the production of sticky and
blunt ends.The DNA sequences used in the construction of
recombinant DNA molecules can originate from any species. For
example, plant DNA may be joined to bacterial DNA, or human DNA may
be joined with fungal DNA. In addition, DNA sequences that do not
occur anywhere in nature may be created by the chemical synthesis
of DNA, and incorporated into recombinant molecules. Using
recombinant DNA technology and synthetic DNA, literally any DNA
sequence may be created and introduced into any of a very wide
range of living organisms.Proteins that can result from the
expression of recombinant DNA within living cells are termed
recombinant proteins. When recombinant DNA encoding a protein is
introduced into a host organism, the recombinant protein is not
necessarily produced. Expression of foreign proteins requires the
use of specialized expression vectors and often necessitates
significant restructuring of the foreign coding
sequence.Recombinant DNA differs from genetic recombination in that
the former results from artificial methods in the test tube, while
the latter is a normal biological process that results in the
remixing of existing DNA sequences in essentially all
organisms.
1.3 Methods of Making Recombinant rDNA
Molecular cloning is the laboratory process used to create
recombinant DNA. It is one of two widely used methods (along with
polymerase chain reaction, abbr. PCR) used to direct the
replication of any specific DNA sequence chosen by the
experimentalist. The fundamental difference between the two methods
is that molecular cloning involves replication of the DNA within a
living cell, while PCR replicates DNA in the test tube, free of
living cells.Formation of recombinant DNA requires a cloning
vector, a DNA molecule that replicates within a living cell.
Vectors are generally derived from plasmids or viruses, and
represent relatively small segments of DNA that contain necessary
genetic signals for replication, as well as additional elements for
convenience in inserting foreign DNA, identifying cells that
contain recombinant DNA, and, where appropriate, expressing the
foreign DNA. The choice of vector for molecular cloning depends on
the choice of host organism, the size of the DNA to be cloned, and
whether and how the foreign DNA is to be expressed. The DNA
segments can be combined by using a variety of methods, such as
restriction enzyme/ligase cloning or Gibson assembly.In standard
cloning protocols, the cloning of any DNA fragment essentially
involves seven steps: (1) Choice of host organism and cloning
vector(2) Preparation of vector DNA(3) Preparation of DNA to be
cloned(4) Creation of recombinant DNA(5) Introduction of
recombinant DNA into the host organism(6) Selection of organisms
containing recombinant DNA(7) Screening for clones with desired DNA
inserts and biological properties.
In a conventional molecular cloning experiment, the DNA to be
cloned is obtained from an organism of interest, and then treated
with enzymes in the test tube to generate smaller DNA fragments.
Subsequently, these fragments are then combined with vector DNA to
generate recombinant DNA molecules. The recombinant DNA is then
introduced into a host organism (typically an easy-to-grow, benign,
laboratory strain of E. coli bacteria). This will generate a
population of organisms in which recombinant DNA molecules are
replicated along with the host DNA. Because they contain foreign
DNA fragments, these are transgenic or genetically modified
microorganisms (GMO). This process takes advantage of the fact that
a single bacterial cell can be induced to take up and replicate a
single recombinant DNA molecule. This single cell can then be
expanded exponentially to generate a large amount of bacteria, each
of which contain copies of the original recombinant molecule. Thus,
both the resulting bacterial population, and the recombinant DNA
molecule, is commonly referred to as "clones". Strictly speaking,
recombinant DNA refers to DNA molecules, while molecular cloning
refers to the experimental methods used to assemble them.
1.4 Functions of rDNA
Ribosomal DNA (rDNA) is a DNA sequence that codes for ribosomal
RNA. Ribosomes are assemblies of proteins and rRNA molecules that
translate mRNA molecules to produce proteins. rDNA of eukaryotes
consists of a tandem repeat of a unit segment, an operon, composed
of NTS, ETS, 18S, ITS1, 5.8S, ITS2, and 28S tracts. rDNA has
another gene, coding for 5S rRNA, located in the genome in most
eukaryotes. 5S rDNA is also present in tandem repeats as in
Drosophila. In the nucleus, the rDNA region of the chromosome is
visualized as a nucleolus, which forms expanded chromosomal loops
with rDNA. These rDNA regions are also called nucleolus organizer
regions, as they give rise to the nucleolus. In the human genome
there are 5 chromosomes with nucleolus organizer regions:
chromosomes 13,14,15,21 and 22.When the recombinant DNA enters the
host cell, the host cell starts expressing the proteins present in
the rDNA. If the expression factors are added along with the rDNA
then host cell will be able to produce significant amount of
proteins. Expression of the protein will not appear until there are
some signals in the host cells. There are specific signals for
every species of bacteria for example; E. coli does not get the
signals of human terminators and promoters.
1.5 Importance of Recombinant DNA
Recombinant DNA is very helpful in techniques like gene therapy.
It is helpful in curing different diseases like cancer. Healthy
genes are inserted in the body and they replace the defected genes.
Some other important features of recombinant DNA are that it can
give better yield of crops. Disease like sickle cell anemia and
hemophilia can be treated with recombinant DNA because it produces
clotting factors. Scientists have successfully produced insulin
with the help of recombinant DNA. Pharmaceutical industry has taken
advantage of rDNA by making drugs. Recombinant DNA has enabled
plants to make their own insecticides.The recombinant DNA
technology (rDNA) is utilized mainly for two types of cloning
namely reproductive and therapeutic cloning. Reproductive cloning
will create a life form with the same genetic information of the
one that exists already. This technique has been already carried
out with some animals. A sheep known as Dolly was the first mammal
to be reproduced as a precise genetic copy. Therapeutic cloning is
utilized in the reproduction of certain tissues or organs and not a
complete organism.Utilization of recombinant DNA technology for the
purpose of therapeutic cloning has immense deal of benefits. For
instance, an organ that is cancerous could be replaced with a new
one prepared from the own DNA of the patient. This would possibly
help to minimize the rejection of organs that occurs occasionally
when a transplant of the organ is carried out. If an organ like
heart is injured, it could even be replicated with the aid of this
technology. Despite the fact that these applications may be many
years from practical use, they are future possibilities.
1.6 Motivation
The motivation of this experiment is to help humans to look
young without going through operations, injection, medication and
suffering from any side effects. As we know, one will lose
self-confidence if they are not happy with their appearance. One
will also keep a distance from friends and society as they have low
self-esteem. So, this experiment is conducted to help humans
suffering from this problem as everybody in this world wish to look
young and beautiful forever and always.
1.7 Justification
Have you ever dream to have a forever young and beautiful look?
It's never too late to reverse the effects of aging. Start now!This
proposal is important because its a one-stop station to maintain
everlasting young and beautiful look. It helps to sustain young and
beautiful look by the process of recombinant DNA sequence in the
neuron and human cells. Hence, we dont need to take the risk of
having surgery to maintain a young good-looking face. This proposal
provides us a better and safe way to sustain a young look.Besides
that, when the DNA of human being combine with the neuron DNA
sequence, our body will automatically produce a hormone which is
able to maintain young looks in human. Last but not least, the cost
of this process is low as its a one-time process. This is because
we want to benefit people from different background and different
level of incomes. Lastly, our products can help to rebuild the
confidence and self-esteem of mankind. In a nutshell, our product
is very important to contribute to society.
2.0 Objective2.1 Objective of Invention of Anti-Aging
Medicine
The purpose of this area is to diminish the ageing process and
reactivate ones health potential, not just by foreseeing or
reverting early ageing after diagnosis, but by naturally
stimulating and rebuilding the processes and metabolic systems
needed in every particular situation, aiming to enjoy of this stage
of life with health and vitality, avoiding illnesses and foods that
ageing bears.Specific objectives: Identification of the reduced
activity and deteriorated organs, to start with the recovering
treatment Prevention and control of a wide range of illnesses
Identification of stress levels and the correction of the same
Identification of toxicity and the providing of solutions to the
same Chelation of the organisms metals Prevention and correction of
muscularskeleton problems, through Global postural reeducation
(RPG)Personalized genetic analysis aiming to improve: Different
cellular activities against free radicals main cause of ageing and
environmentally induced diseases, like the majority of cancers
Cardiovascular system with specific anti-atherosclerosis,
anti-thrombosis and other individual measures Glucose metabolism
and diabetes prevention Weight control and physical activity Brain
activity Bone metabolism and osteoporosis Skin health
(dermagenetics) Anti-fatigue Personalized nutrition followed by
strong rejuvenation effect (nutrigenomics) Bio-identical hormonal
replacement therapy (same molecular structure as the one produced
by our organism)2.2 To Extract DNA from Human DNA extraction
discusses what DNA is and how it relates to genes and chromosomes.
DNA extraction contributes in processes of: Visualize the
relationship between DNA, genes, and chromosomes. Compare the roles
that DNA and proteins play in a cell. Explain how proteins are made
from DNA (the processes of transcription and translation). Contrast
DNA and proteins in their chemical make up. Explain why DNA
extraction is important in genetic engineering and how it is done.
Understand why genes can be transferred between organisms and still
workIn our experiment, we would to extract the gene that cause
aging in human and take out that particular gene and replace
it.
2.3 Exchange in Genetic MaterialsI. IntroductionIn bacterial
populations mutations are constantly arising due to errors made
during replication. If there is any selective advantage for a
particular mutation (e.g. antibiotic resistance), the mutant will
quickly become the major component of the population due to the
rapid growth rate of bacteria. In addition, since bacteria are
haploid organisms, even mutations that might normally be recessive
will be expressed. Thus, mutations in bacterial populations can
pose a problem in the treatment of bacterial infections. Not only
are mutations a problem, bacteria have mechanisms by which genes
can be transferred to other bacteria. Thus, a mutation arising in
one cell can be passed on to other cells. Gene transfer in bacteria
is unidirectional from a donor cell to a recipient cell and the
donor usually gives only a small part of its DNA to the recipient.
Thus, complete zygotes are not formed; rather, partial zygotes
(merozygotes) are formed.Bacterial genes are usually transferred to
members of the same species but occasionally transfer to other
species can also occur. Figure 1 illustrates gene transfers that
have been shown to occur between different species of bacteria.
II. Gene Transfer Mechanisms in BacteriaA. Transformation
Transformation is gene transfer resulting from the uptake by a
recipient cell of naked DNA from a donor cell. Certain bacteria
(e.g. Bacillus, Haemophilus, Neisseria, Pneumococcus) can take up
DNA from the environment and the DNA that is taken up can be
incorporated into the recipient's chromosome.
1. Factors affecting transformationa. DNA size state Double
stranded DNA of at least 5 X 105 daltons works best. Thus,
transformation is sensitive to nucleases in the environment.b.
Competence of the recipient Some bacteria are able to take up DNA
naturally. However, these bacteria only take up DNA a particular
time in their growth cycle when they produce a specific protein
called a competence factor. At this stage the bacteria are said to
be competent. Other bacteria are not able to take up DNA naturally.
However, in these bacteria competence can be induced in vitro by
treatment with chemicals (e.g. CaCl2)
2. Steps in transformationa. Uptake of DNA Uptake of DNA by
Gram+ and Gram- bacteria differs. In Gram + bacteria the DNA is
taken up as a single stranded molecule and the complementary strand
is made in the recipient. In contrast, Gram- bacteria take up
double stranded DNA.b. Legitimate/Homologous/General Recombination
After the donor DNA is taken up, a reciprocal recombination event
occurs between the chromosome and the donor DNA. This recombination
requires homology between the donor DNA and the chromosome and
results in the substitution of DNA between the recipient and the
donor as illustrated in Figure 2.
Figure 2
Recombination requires the bacterial recombination genes (recA,
B and C) and homology between the DNA's involved. This type of
recombination is called legitimate or homologous or general
recombination. Because of the requirement for homology between the
donor and host DNA, only DNA from closely related bacteria would be
expected to successfully transform, although in rare instances gene
transfer between distantly related bacteria has been shown to
occur.
3. SignificanceTransformation occurs in nature and it can lead
to increased virulence. In addition transformation is widely used
in recombinant DNA technology.
2.4 To Produce a New Recombinant DNARecombinant DNA technology
is joining together of DNA molecules from two different species
that are inserted into a host organism to produce new genetic
combinations that are of value to science, medicine, agriculture,
and industry. Since the focus of all genetics is the gene, the
fundamental goal of laboratory geneticists is to isolate,
characterize, and manipulate genes. Although it is relatively easy
to isolate a sample of DNA from a collection of cells, finding a
specific gene within this DNA sample can be compared to finding a
needle in a haystack. Consider the fact that each human cell
contains approximately 2 meters (6 feet) of DNA. Therefore, a small
tissue sample will contain many kilometers of DNA. However,
recombinant DNA technology has made it possible to isolate one gene
or any other segment of DNA, enabling researchers to determine its
nucleotide sequence, study its transcripts, mutate it in highly
specific ways, and reinsert the modified sequence into a living
organism.
2.5 Human Anti-Aging Gene"No pain, no gain" is the mantra of
most diet and exercise programs. However, since a severely
restricted diet isn't a good long-term solution for most people,
scientists have been trying to find a way to create those same
results without actually cutting the calories. What could trigger
the body into thinking that it's consuming fewer calories?Dr.
Leonard P. Guarente, a biology professor at M.I.T., hit upon a
potential answer when he was studying yeast cells in the mid 1990s.
As expected, the cells lived longer when they were given very small
amounts of food, and Dr. Guarente began manipulating the cells'
genes to determine what part they played in the extended life span.
When yeast cells undergoing caloric restriction were endowed with
one certain gene, they lived even longer, and when that gene was
eliminated by Dr. Guarente, the caloric restriction was for naught,
and the yeast cells died. That gene was silent information
regulator No. 2, or SIR2.SIR2 appeared to stop the aging process by
stopping the production of waste material in the cell, which
allowed the cell to work better for longer. Dr. Guarente was able
to duplicate his results with another small organism, the
roundworm, which demonstrated that this gene played a role in
extending longevity during periods of caloric restriction in
several different species. But what of humans?It turns out humans
don't have SIR2, but we have a gene that appears to do the same
thing: SIRT1. Both SIR2 and SIRT1 seem to work the same way in the
body; they're charged with repairing DNA within the body and
suppressing certain genes. Gene silencing, as this suppression is
called, is important because if the wrong genes become activated,
then the cell's function could be destroyed. It may be that cases
of Alzheimer's and diabetes occur because of this type of genetic
malfunction.Dr. Guarente believes that as we age, it's harder for
SIR2 and SIRT1 (collectively known as sirtuins) to multitask, so
that this gene silencing falls by the wayside. As a result, we end
up with the conditions we associate with old age, like cancer,
heart disease and the aforementioned Alzheimer's and diabetes. It
seems that caloric restriction is so effective because it helps
sirtuins work better within the body.Still, if a calorie restricted
diet is unrealistic, then how does knowing this help us live
longer?
2.6 Anti-Aging FirewallsThe Science and Technology of LongevityA
comprehensive document for the benefit of people interested in
living very long healthy lives and who are willing to adapt
emerging knowledge personally to do so. And, for the health
professionals who serve them.
PREFACE More than five years have elapsed from drafting the
initial version of this treatise. The original concept of this
treatise was to look at the main existing scientific theories of
aging, see what they have in common, see what each has to say about
steps that could be taken to halt or delay aging, and combine these
steps into an overall "antiaging firewall." That firewall would
define practical lifestyle and dietary interventions that would
create long-lasting health and longevity based on the known
science. I still believe this was a good concept. However, since
then, my basic perspective about health and aging has shifted
significantly and become greatly more sophisticated. Originally, I
thought that I could continue to update this treatise as I followed
the key scientific streams related to health and aging and learned
more. Soon, I discovered that for older people, creating health and
creating longevity amount to the same thing. And, to know how to do
that based on new scientific discoveries, it was necessary to
consider vast, disparate and detailed bodies of scientific
knowledge. Over 1 million potentially relevant scientific papers
are now published every year.It would be completely impossible to
encompass even summaries of the relevant knowledge in this one
treatise. So, I created the blog agingsciences.com as a vehicle for
communicating about particularly relevant topics. The blog became
my main vehicle for writing up what I have learned. It served the
initial objective of making sure that I understand a topic by
forcing me to lay it out in writing in comprehensive form. Soon, a
second objective emerged for the blog, which was communicating this
information to a wider audience, get feedback and network myself
with other researchers. The blog became my major focus of activity,
with further updating of this treatise as increasingly secondary.
As time has progressed I have found my appreciation and
understanding of the detailed sciences involved in aging and health
have multiplied manyfold. And yet, the more I learn the more
obvious it is that there is much more yet to be learned. It seems
that for everything I learn, I discover there are two new things
yet to be learned.At first, few people read the blog, but over the
years its readership as well as the attention it has received from
the scientific community have been increasing exponentially.
Early-on, I started posting longer blog posts that go into
considerable depth and have been updating this treatise less
frequently. The blog now (October 24, 2013) includes over 460 posts
and some 2,000 comments. On the average, 3,600 to 4,000 readers
access the blog daily, with an average of 2.4 blog entries viewed
per user access. And there are now over 26,000 registered blog
subscribers, up from 12,000 users in mid-May of this year. New
registraants are coming in at a rate of nearly 1,000 a week. About
half of the usage is international. Other strong and highly
informed intellectual contributors have joined me in researching
and authoring materials for the blog, Jim Watson in particular. And
as time has progressed Im spending more and more time researching
and communicating with other researchers and relatively less time
actually writing for the blog or working on this treatise.I have
been attempting to update this treatise with regard to its central
content as time progresses - including selected links from this
treatise to blog entries that amplify on particularly relevant
points only very-selectively. However, a large number of important
topics, mainly ones of newer science, are not effectively treated
here, but are covered fairly comprehensively in blog entries. These
include progress in stem cell research, many topics of epigenetics,
several key gene-activation pathways, mitochondrial dynamics, redox
related pathways, health-producing properties of plant polyphenols,
stress-responses and hormesis, quorum sensing in biofilms,
bacterial communications, nano delivery of therapeutic substances,
quantum biology and systems biology, human bacterial biomes,
age-related diseases including Alzheimers, Parkinsons, diabetes and
cancers, evolutionary origins of our signaling systems,, exosomal
communication systems, cell senescence, and signaling gasses - to
mention just a few. Readers with particular interests are invited
to check over the listings of blog entries included here. You can
use your browsers search function on this page to find and link to
particular entries.As to shift over time of my overall perspective,
a central observation is that I no longer view the theories of
aging described here as independent or even necessarily
fundamental. They are all part of an emerging new grand unified
theory (GUT) of biology. For example, REDOX processes, central to
the first theory of aging, actually play significant roles in each
of the other theories. Some of the theories are more basic and
upstream of the others. Some like lipofuscin accumulation, telomere
shortening and tissue glycation and even cancers and heart diseases
are definitely downstream in the causal chain. I expect to be
forwarding the development of that GUT in close cooperation with
Jim Watson, and at some point this will become the subject of a new
book.Another key observation is the importance of researching and
drawing together discoveries from across a wide spectrum of
disciplines be the publications drawn from the literatures of
genetics, epigenetics, cancer research, research in other specific
diseases, cell components like mitochondria or microtubules, stem
cells, plant biology, dose-responses, biogerentology, biochemistry
of proteins, etc. Relatively few of our citations are drawn from
the works of researchers primarily involved in the field of aging.
Sadly but probably necessarily, most researchers work in
disciplinary areas where there is great emphasis on depth of detail
but where there is little time to encompass or integrate in
discoveries from other disciplines. I believe the blog has been
able to surface a number of important original insights by bringing
together and interpreting discoveries from different disciplines in
new contexts.I continue to see the value of this treatise mainly as
a source document for somebody who wants to begin the process of
learning about aging and longevity research, and who is concerned
with practical steps, implementable today, that may be likely to
extend their healthy lifespans.
2.7 The Ways to Solve Problems FacedAllelic exchange experiments
allow investigation of the functions of many unknown genes identied
during the sequencing of entire genomes. Isogenic strains differing
by only specic mutations can be constructed. Among other tools,
suicide plasmids are widely used for this task. They present many
advantages because they leave no scars on the chromosome, and
therefore allow combining several mutations in the same genetic
background. While using the previously described pCVD442 suicide
plasmid [Infect. Immun. 59 (1991) 4310], we found untargeted
recombination events due to the presence of an IS1 element on this
plasmid. The plasmid was therefore improved by removal of the IS1.
We also replaced the bla gene of pCVD442, conferring ampicillin
resistance, by the cat gene conferring chloramphenicol resistance,
leading to the new suicide plasmid pDS132. The plasmid was entirely
sequenced. We demonstrate that this new vector can be easily used
to introduce various types of mutations into dierent genetics
backgrounds: removal of IS elements, introduction of point
mutations or deletions. It can be introduced into bacterial strains
by either transformation or conjugation.
3.0 Method3.1 Skin Cell as A Source of Neurons
As all of us know skin cell is one of the cell that most
actively dividing hence Columbia University (New York, USA)
researchers have successfully generated functional neurons directly
from human skin cell through the process of trial and error.1.
Identified a cocktail of factors that could turn human skin cells
into neurons.2. Experiment is carried out in dish of nutrient
containing medium, replicate neurons could fire and receive signals
just like normal neurons without any side effect3. The neuron from
skin cell is placed into the brains of developing mice.4. The
converted cell able to connect up with the existing circuitry and
it will function normally for 25 yearsBy this method we can
regenerate our brain neurons as we can do major neuron transfusion
operation at the age of 45 to 50 hence the neuron will
interconnected with existing neuron so that our brain will function
effectively.
3.2 Treatments and CureSome, as yet unpublished, stem cell
research is looking at Zebra fish for answers, as they are able to
regenerate injured nerve cells. Scientists speculate about future
nerve stem cell harvesting and growth in laboratories, then
transplantation to regrow motor neurons. In animal studies, stem
cells delayed motor neuron degeneration. This research might also
provide clues for the development of nerve cell regeneration
boosting medication.The only conventional medication proven to slow
the disease is riluzole, which suppresses the glutamate secretion
and retards the death of nerve cells, although its modest effects
only prolong survival by 2-4 months.In integrative medicine, hope
was that certain strong antioxidants would help. But a Cochrane
Database review of a range of studies couldnt find enough evidence
to support their benefits in treating MND. However, only vitamin C,
vitamin E, acetlycysteine, L-methionine and selenium were included
in the review, so the lack of the evidence doesnt necessarily prove
theyre completely ineffective. Researches admit to poorly designed
studies with results being not 100%t trustworthy.Evidence suggests
that MND associated nerve cell death is partly due to low levels of
the antioxidant glutathione, which protects cells from toxins and
free radicals. Treatment with intravenous glutathione, combined
with a phospholipid exchange therapy that strengthens weakened cell
membranes, may offer of a way of slowing the diseases
progress.There have also been reports of success with slowing or
halting MNDs progress with low-dose naltrexone (LDN), a medicine
used in higher doses to treat drug addictions. LDN treatment is
regarded as experimental, though, and requires clinical studies to
support the positive anecdotal reports.
4.0 Expected Results
This Neuronal Anti-Aging Recombination (NAAR) is expected to
last a lifetime in human body. NAAR will replicate itself as the
cell replicates. NAAR will produce hormone that will help to
sustain young and beautiful look. NAAR is highly recommended, as we
need not undergo expensive and risky operation to have young and
beautiful look. In order to be accepted in the worldwide for the
use of genetic engineering, NAAR must be accepted worldwide. The
NAAR is hope to give a positive and effective result to maintain
healthy and young-looking skin. It is considered safe to be used
and does not bring any side effects to the consumers. Needless to
say that, NAAR can bring out and maintain the beauty of each human
being, which helps to build confidence and self-esteem in human
beings. As a result, human beings are encourage to use NAAR to
maintain young and beautiful look.
5.0 Reference
http://health.howstuffworks.com/wellness/aging/anti-aging-tips/anti-aging-gene1.htm
http://pathmicro.med.sc.edu/mayer/genetic%20ex.htm
http://people.csail.mit.edu/tk/chromosome-editing/Philippe04.pdf
file:///Users/sylviachong/Desktop/Bio%20Assignment/Motor%20Neuron%20Disease.html
Spyridopoulos I et al. Arteriosclerosis, Thrombosis & Vascular
Biology. 28(5):968-974, May 2008 Jos J. Fuster, Vicente
Andrs.Circulation Research. 2006;99:1167.2006 American Heart
Association, Inc.Reviews.Telomere Biology and Cardiovascular
Disease Ignacio Flores, Roberta Benetti and Maria A Blasco.
Telomerase regulation and stem cell behaviour. Current Opinion in
Cell Biology 2006, 18:254260 Frederick M. Rauscher et al.Aging,
Progenitor Cell Exhaustion, and Atherosclerosis. Circulation, The
American Heart Association TL Limke, MS Rao, Neural stem cell
therapy in the aging brain: pitfalls and possibilities. J
Hematother Stem Cell Res (2003) 12: 615-23 Zouboulis CC, Adjaye J,
Akamatsu H, Moe-Behrens G, Niemann C.Human skin stem cells and the
ageing process. Exp Gerontol. 2008 Sep 9 Ignacio Flores, Roberta
Benetti and Maria A Blasco. Telomerase regulation and stem cell
behaviour. Current Opinion in Cell Biology 2006, 18:254260
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