Amyloid plaques are clumps of protein fragments
called amyloid beta (Aβ) that accumulate between nerve cells (neurons) in the
brains of individuals with Alzheimer's disease (AD). These plaques are a
hallmark pathology of AD and are believed to contribute to the progressive
cognitive decline and neurodegeneration associated with the disease.
In a healthy brain, Aβ is normally broken down
and eliminated. However, in AD, Aβ peptides aggregate and form insoluble
plaques. These plaques can disrupt communication between neurons, interfere
with cellular functions, and trigger inflammatory responses, ultimately leading
to neuronal damage and cell death.
The presence and density of amyloid plaques in
the brain are used as diagnostic markers for AD, often detected through imaging
techniques like PET scans or by examining brain tissue post-mortem.
Current research focuses on understanding the
mechanisms of Aβ accumulation, developing treatments to reduce plaque formation
or enhance their clearance, and investigating their role in the cascade of
events that lead to cognitive impairment in Alzheimer's disease.
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