PATHOGENESIS OF ALZHEMEIR'S

Pathogenesis:

From brain atopsy studies, Alzeimers disease patients have been found to have cortical atropy, a significant loss a neurons ,an increase in neuritic plaques, and a high density of neurofibrillary tangles, Neurofibrillary tangles are abnormal neurons containing bundles of filamentous structures in the cytoplasm.

Tangles destroy a vital cell transport system made of proteins. This electron microscope picture shows a cell with some healthy areas and other areas where tangles are forming.

In healthy areas:

·         The transport system is organized in orderly parallel strands somewhat like railroad tracks. Food molecules, cell parts and other key materials travel along the “tracks.”

·         A protein called tau (rhymes with wow) helps the tracks stay straight.

In areas where tangles are forming:

·         Tau collapses into twisted strands called tangles.

·         The tracks can no longer stay straight. They fall apart and disintegrate.

·         Nutrients and other essential supplies can no longer move through the cells, which eventually die.These filaments are are wound around each other in a helical fashion.

Neuritic plaques are small spheres with an amyloid protein core surrounded by degenerating nerve terminals .Two Amyloid proteins, Beta amyloid and paired helical filament protein are present in those hallmark lesions and may be linked to the cause of alzeimers disease.

Plaques form when protein pieces called beta-amyloid (BAY-tuh AM-uh-loyd) clump together. Beta-amyloid comes from a larger protein found in the fatty membrane surrounding nerve cells.

Beta-amyloid is chemically "sticky" and gradually builds up into plaques.

The most damaging form of beta-amyloid may be groups of a few pieces rather than the plaques themselves. The small clumps may block cell-to-cell signaling at synapses. They may also activate immune system cells that trigger inflammation and devour disabled cells.

In autopsy studies, the degeree of plaque formation has been highly correlated with the degree of clinical impairment observed when the patient was alive.