Alzheimer’s disease (AD) is an age-related and irreparable brain disorder that strikes slowly and causes memory loss, behavior and personality changes, and deterioration of mental capacities. These losses are brought about by the collapse of the links between nerve cells in the brain and the ultimate death of most of these cells. The natural course of the disease differs from one person to another also the rate of decline. Typically, patients with AD may live up to 8 to 10 years after they diagnose, and may live as long as 20 years.

What Are the Main Characteristics of AD?

Two noticeable abnormal structures in the brain that characterizes AD are the following: amyloid plaques and neurofibrillary tangles.

There are several changes noticed in the brain afflicted with AD according to the order of appearance:

• The accumulation of an abnormal protein called amyloid beta outside nerve cells in the form of amyloid. These are referred to as diffuse plaques. Amyloid also makes up the hub of more structured plaques called senile or neuritic plaques. Recent studies have shown that simpler, soluble forms of amyloid (oligomers) are involved in the pathological process, and the existence of plaque amyloid does not show a link on the degree of dementia. Amyloid also builds up in the walls of the brain’s small blood vessels which are called amyloid angiopathy or congophilic angiopathy. Another pathological characteristic of AD is the amassing of abnormal protein filaments found inside nerve cells in the brain, formed from clustering of tau protein. Presence of tau proteins serves to stabilise microtubules. In AD, an oddly phosphorylated form of tau protein gathers as paired helical filaments.

The tau accumulates in several forms:
• As heaps of filaments found inside nerve cell body called neurofibrillary tangles
• Found within nerve cell processes in the brain referred to as neuropil threads
• Inside nerve cell processes surrounding amyloid plaques called dystrophic neurites or plaque neurites

Amyloid Plaques

In AD, plaques form first in parts of the brain that are used for memory and other cognitive functions. They are made up mostly of deposits that cannot be dissolved of beta-amyloid – a piece of protein trimmed from a bigger protein called amyloid precursor protein (APP) – combined with part of neurons and with non-nerve cells such as microglia which are cells that enclose and take in damaged cells or foreign substances that trigger inflammation and astrocytes or glial cells whose main function is to support and feed neurons. Amyloid plaques are located in the spaces between the brain’s nerve cells. Researchers could not ascertain if the amyloid plaques cause AD or if they are brought about by the AD process. There is proof though that amyloid deposition may play a vital process in the disease. Studies show that changes in the composition of the APP protein can result in AD, as observed in one inherited form of AD, which is the result of gene mutations that contains instructions for developing the APP protein. Recent studies are able to uncover the nature of beta-amyloid and the ways in which it may be poisonous to neurons, the processes undergone to form plaques and how they are deposited in the brain, and methods in which the numbers of plaques can be trimmed down.

Neurofibrillary Tangles

The second noticeable characteristic of AD consists of abnormal collections of twisted threads found in the nerve cells. The main component of these tangles is a type of protein termed tau. In the central nervous system, tau proteins primary function is to bind and
help stabilize microtubules or one of the basic components of the cell’s internal support structure, or its skeleton.

In healthy neurons, microtubules creates structures similar to train tracks that function as a guide to nutrients and molecules from the bodies of the cells down to the ends of the axon. Tau is responsible for keeping together the “railroad ties” or connector parts of the microtubule tracks. In AD, however, the tau is altered chemically making forming twists into paired helical filaments or two threads of tau wrap around each other. These filaments accumulate to create neurofibrillary tangles. When this occurs, the tau could no longer hold the railroad tracks together and the microtubules collapse. When the transport system falls apart it results in failure in communication between nerve cells and eventually will result in neuronal death that causes the development of dementia. Recent studies conducted have explained the abnormal accumulation of tau protein and the role that some genetic mutations contribute in altering tau’s structure and causing neurodegeneration.

Gwen Cuizon

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