Memory

• Fact memory

• Skills memory

Cortical Sensory

Area

AmygdalaHippocampus

Diencephalon

PrefrontalCortex

BasalForebrain

CorticalSensory

Area

CorpusStriatum

MotorCortexCerebellum

ExtrapyramidalMotorNuclei

Alzheimer’s

• Features

• Etiology

• Pathophysiology

• Manifestation

• Diagnosis

• All of this is in your lab book!!

Features

• degenerative

• most common dementia

• 4th most common cause of death

• not a normal part of ageing

Etiology

• no gender differences

• risk increases with age– can be 40 - 50– most over 65

• prevalence = 20% by 80

• 10-15% of cases potentially attributed to depression

Etiology

• Slow virus - incubation period 2 - 30 years, transmission difficult to prove

• An auto immune process - increased levels of brain reactive antibodies

• Aluminium toxicity - aluminium deposits have been identified in some patients.

Etiology

• Genetic predisposition - 10 - 30% of patients have familial association

• +ve correlation with fat

• defect on chromosome 21 implicated supported by Downs developing AD in 4th decade

• SDAT families produce 3x normal numbers of Downs children

The 7 Dietary Principles to Reduce Alzheimer's RiskPCRM

• 1. Minimize saturated fats and trans fats.

• 2. Vegetables, legumes (beans, peas, and lentils), fruits, and whole grains should be the primary staples of the diet.

• 3. One ounce of nuts or seeds (one small handful) daily provides a healthful source of vitamin E.

• 4. A reliable source of vitamin B12, such as fortified foods or a supplement providing at least 2.4 μg per day for adults) should be part of the daily diet.

• 5. Choose multivitamins without iron and copper, and consume iron supplements only when directed by your physician.

• 6. Avoid the use of cookware, antacids, baking powder, or other products that contribute dietary aluminium.

• 7. Engage in aerobic exercise equivalent to 40 minutes of brisk walking 3 times per week.

Pathophysiology

• severe loss of hippocampal and cortical neurons (hippocampus becomes isolated and functionless)

• presence of granulovacuolar degeneration, diffuse neurofibrillary tangles and senile plaques

Pathophysiology

• last 2 changes also found in lead encephalopathy and Downs

• suggested that enzymes metabolising neurotransmitters are involved; choline acetyltransferase is reduced

• severity of dementia directly related to reduction in brain ACh

Manifestations

• insidious and progressive loss of memory, disorientation, impaired abstract thinking, changes in personality

• Three stages:

Manifestations

• 1 2 - 4 yrs– subjective memory deficit, random

forgetfulness, get lost easily– lack of spontaneity– subtle personality changes (loss of sense of

humour)– disorientation to time and date

Manifestations

• 2 Confusional - may last several years– impaired cognition and abstract thinking– restlessness and agitation– wandering - "Sundown Syndrome”– inability to carry out daily living activities

Manifestations

• 2 Confusional (cont’d)– impaired judgement– inappropriate social behaviour– lack of insight– repetitive behaviour– voracious appetite

Manifestations

• 3 Terminal - 1 - 2 yrs– indifference to food leads to emaciation– inability to communicate– urinary and faecal incontinence– seizures– death usually the result of malnutrition or

infection

Diagnosis

• absence of definitive test

• diagnosis only by microscopic examination of tissue from cerebral biopsy or autopsy

• patient presenting should be tested to detect potentially reversible nutritional, endocrine, and infectious causes of symptoms (eg. B12 deficiency, thyroid dysfunction and electrolyte imbalance)

Diagnosis

• requires presence of dementia established by clinical examination and documented by results of a Mini-mental status test, Blessed dementia test, or similar to yield deficits in 2 or more areas of cognition and progressive worsening of memory or other cognitive functions