Alzheimer’s disease (AD) is the most prevalent and severe neurodegenerative disease affecting
more than 0.024 billion people globally, more common in women as compared to men. Senile
plaques and amyloid deposition are among the main causes of AD. Amyloid deposition is considered as a
central event which induces the link between the production of β amyloid and vascular changes. Presence
of numerous biomarkers such as cerebral amyloid angiopathy, microvascular changes, senile plaques,
changes in white matter, granulovascular degeneration specifies the manifestation of AD while an aggregation
of tau protein is considered as a primary marker of AD. Likewise, microvascular changes, activation
of microglia (immune defense system of CNS), amyloid-beta aggregation, senile plaque and many
more biomarkers are nearly found in all Alzheimer’s patients. It was seen that 70% of Alzheimer’s cases
occur due to genetic factors. It has been reported in various studies that apolipoprotein E(APOE) mainly
APOE4 is one of the major risk factors for the later onset of AD. Several pathological changes also occur
in the white matter which include dilation of the perivascular space, loss of axons, reactive astrocytosis,
oligodendrocytes and failure to drain interstitial fluid. In this review, we aim to highlight the various
biological signatures associated with the AD which may further help in discovering multitargeting drug
therapy.
Chronic hypoperfusion due to intracranial large artery stenosis is not associated with cerebral β-amyloid deposition and brain atrophy
