Causes

There are no definitive causes of AD. Some that have been identified include
lesions caused by plaque, inflammation in brain cells, oxidative stress
effects on brain cells, genetic factors, beta amyloid protein and senile
plaques, tau protein and neurofibrillary tangles, estrogen effects on brain neurotransmitters, dysfunction in brain cell communication, autoimmune
responses, viruses, and vessel anomalies.
plaque. In AD, plaques develop in the areas of the brain that regulate
memory and other cognitive functions. These plaques are deposits of betaamyloid
(a protein fragment from a larger protein called amyloid precursor
protein, APP) intermingled with portions of neurons and with nonnerve cells
such as microglia (cells that surround and digest damaged cells or foreign substances)
and astrocytes (glial cells that support and nourish neurons). Plaques
are found in the spaces between the brain’s nerve cells. Researchers do not
know whether amyloid plaques causeADor are a by-product of theADprocess.
AD consists of abnormal collections of twisted threads found inside nerve
cells. The chief component is a protein called tau. In the central nervous system,
tau proteins bind and stabilize brain cells’ support structure by forming
tubules that guide nutrients and molecules from the cells to the ends of
the axon. Tau normally holds together connector pieces of the tubule
tracks. In AD, tau threads twist around each other and form neurofibrillary
tangles. Support to the cell is lost, causing cell death and leading to dementia.