Pharmacological Treatment Involved In Alzheimers Disease Biology

Alzheimers disease discovered by the German neurologist Alois in 1906 is a progressive degenerative brain disease and has no known cure. Alzheimer's disease is the breakdown and destruction of brain cells. Since the brain is the central command station of the body, a breakdown in cells comes with the loss of everyday functions such as speech and memory. In Alzheimer's disease parts of the brain nerve cells (cholinergic neurons) become damaged. Their breakdown begins to problems in other areas of the brain. As the damage spreads, cells lose their ability to support brain functions. Eventually, the brain cells die. Two microscopic abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques build up between nerve cells. They contain deposits' of a protein fragment called beta-amyloid. Tangles are twisted fibres of another protein called tau [1].

However, the exact causes of Alzheimer's disease are not known yet, but there are three major hypotheses. There is the cholinergic hypothesis, which proposes that Alzheimer's disease is caused by reduced synthesis of the neurotransmitter. The amyloid hypothesis postulated that amyloid beta deposits are the fundamental cause of the disease where as the tau protein hypothesis leading to the formation of neurofibrillary tangles.

The cholinergic hypothesis started when patients with Alzheimer's disease where found to have up to 90% decrease in acetylcholinesterase and choline acetyltransferase activity. Acetylcholinesterase (AChE) is an enzyme, which terminates the cholinergic nerve transmission. AChE is found in the post-synaptic membrane of cholinergic synapses, where it binds with acetylcholine, which gets hydrolysed to acetate and choline. This inactivates acetylcholine causing the nerve impulse to be halted (see fig1.0). Choline acetyltransferase (CAT), on the other hand is an enzyme which catalyses the acetycholine synthesized from acetyl-coA and choline in the cytoplasm of autonomic nerve terminals. However in Alzheimer's disease CAT is less active than in non-Alzheimer's brain resulting in a reduction in the synthesis of Ach. As CAT activity declines, less Ach is packaged into the synaptic vesicles and released at the nerve terminal. This deficit in Ach leads to decreased neurotransmission and is implicated in the pathogenesis of Alzheimer's disease (see fig1.1)

(Fig1.0: The mechanisms action

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