Dementia

Deficits In:

• Memory
• Language
• “Executive Functions”

Also:

• Apraxia
• Agnosia (e.g., prosopagnosia)

Structural Deficits in Alzheimer’s:

• Neurofibrillary tangles
• Senile plaques

Etiology

Aluminum

• Rabbits exposed to toxic levels of aluminum developed neurofibrillary tangles
• Not supported in humans
• However, dialysis dementia associated with high levels of aluminum
• But no neurofibrillary tangles

Immune System

• Amyloid is a product of immune system cells
• Dysfunctional immune system A
• Amyloid bodies (senile/neuritic plaques)?

Viral

• Not yet possible to transmit Alzheimer’s to animals by injection of Alzheimer’s brain tissue
• Viral infection not proved, but still possible
• Should handle brain tissue appropriately
• Exclude patients from blood donation

Defect in Microtubular Function During Development

• Higher incidence of down’s syndrome in families of Alzheimer’s patients
• Down’s syndrome caused by microtubular dysfunction
• Abnormal mitosis of down’s syndrome
• Related to neurofibrillary pathology in Alzheimer’s patients?

Genetics

• 50% prevalence of Alzheimer’s among 1st degree relatives
• Suggests autosomal dominant heredity in majority of the cases

Traumatic Brain Injuries

• Contributing factor?

Effects of Strokes

• CVAs – cerebrovascular accidents
• Seem to have compounding effect

Diagnosis:

• Possible, probable, or definite (see handout)

Treatment:

• There is no cure for Alzheimer’s

Tacrine (cognex), Aricept

• Acetylcholinesterase inhibitor
• Prevents the degradation of endogenously released acetylcholine

Problem With Cognex

• High risk of liver dysfunction
• Must be monitored
• Results statistically significant for 30-week follow-up
• Clinical significance?
• Disorder not cured, just slowed

Multi-Infarct Dementia

• Stepwise Decline
• Patchiness of Deficits
• Awareness may be preserved

Delirium

• Visual Hallucinations
• Abrupt Onset
• Associated with Medical Condition
• Fluctuating Course
• Impaired attention