Alzheimer's disease.

Alzheimer's disease. ✓

(1) Alzheimer's disease is the most common form of dementia. 

(2) Its incidence increases with the age. 

(3) Symptoms include loss of cognitive thinking, remembering, functioning, reasoning and behavioral abilities. It interferes with the person's daily life and activities. 

 (4) It occurs due to loss of cholinergic and other neurons in the CNS and accumulation of amyloid proteins. 

 (5) There is no cure for Alzheimer's, but treatment slows down the progression of the disease and may improve the quality of life.

Alzheimer’s disease (AD) (ALTZ-hı¯-merz) is a disabling senile dementia, the loss of reasoning and ability to care for oneself, that afflicts about 11% of the population over age 65. In the United States, about 4 million people suffer from AD. Claiming over 100,000 lives a year, AD is the fourth leading cause of death among the elderly, after heart

disease, cancer, and stroke. The cause of most AD cases is still unknown,

but evidence suggests it is due to a combination of genetic factors,

environmental or lifestyle factors, and the aging process. Mutations in

three different genes (coding for presenilin-1, presenilin-2, and amyloid

precursor protein) lead to early-onset forms of AD in afflicted families

but account for less than 1% of all cases. An environmental risk factor

for developing AD is a history of head injury. A similar dementia occurs

in boxers, probably caused by repeated blows to the head.

Individuals with AD initially have trouble remembering recent events. They then become confused and forgetful, often repeating questions or getting lost while traveling to familiar places.

Disorientation grows, memories of past events disappear, and episodes of paranoia, hallucination, or violent changes in mood may occur. As their minds continue to deteriorate, they lose their ability to read, write, talk, eat, or walk. The disease culminates in dementia.

A person with AD usually dies of some complication that afflicts bedridden patients, such as pneumonia.

At autopsy, brains of AD victims show three distinct structural

abnormalities:

1. Loss of neurons that liberate acetylcholine. A major center of

neurons that liberate ACh is the nucleus basalis, a group of large cells below the globus pallidus. Axons of these neurons project widely throughout the cerebral cortex and limbic system. Their

destruction is a hallmark of Alzheimer’s disease.

2. Beta-amyloid plaques (baˉ-ta-AM-i-loyd), clusters of abnormal proteins deposited outside neurons.

3. Neurofibrillary tangles (noo-roˉ-FI¯-bril-ler-e¯), abnormal bundles of

filaments inside neurons in affected brain regions. These filaments consist of a protein called tau (TAW) that has been hyperphosphorylated (hı¯-per-fos-FOR-i-laˉ-ted), meaning too many phosphate

groups have been added to it.

Drugs that inhibit acetylcholinesterase (AChE), the enzyme that inactivates ACh, improve alertness and behavior in about 5% of AD patients. Tacrine®, the first anticholinesterase inhibitor approved for treatment of AD in the United States, has significant

side effects and requires dosing four times a day. Donepezil®, approved in 1998, is less toxic to the liver and has the advantage of

once-a-day dosing. Some evidence suggests that vitamin E (an ant ioxidant), estrogen, ibuprofen, and ginkgo biloba extract may have

slight beneficial effects in AD patients. In addition, researchers are

currently exploring ways to develop drugs that will prevent betaamyloid plaque formation by inhibiting the enzymes involved in

beta-amyloid synthesis and by increasing the activity of the enzymes involved in beta-amyloid degradation. Researchers are also

trying to develop drugs that will reduce the formation of neurofibrillary tangles by inhibiting the enzymes that hyperphosphorylate tau.