ALZHEIMER’S DISEASE AND PATHOLOGICAL ANGIOGENESIS

In spite of huge investigations, the pathology of Alzheimer’ sdisease (AD) is uncertain. Vessels dysfunction is a critical mark of AD. Research has stated like beta-amyloid (Aβ) results augmented vascular development in brains, a pathway observed in AD patients. In AD, cerebral endothelium releases pro substances for β-amyloid plaque and neurotoxins that kill cortical neurons. Vascular vulnerable features and neural, vascular dysfunction related through hypo or hypertension, hypercholesterolemia, diabetes mellitus, smoking, oxidative stress, and iron overload have been invented to play essential parts in the pathogenesis of stroke and AD. Antiangiogenic agents and small molecule kinase blockers are being examined and approved for anticancer therapy and showed normal blood vessel growth in the affected areas. Endothelial cells (EC) are triggered by the angiogenesis of cerebral ischemia and hypoxia. Outcomes of epidemiological research show that chronic administration of NSAIDs, statins, H₂ antihistamines, or calcium-channel blocker sappearstoavert AD. This is mainly due to the ability of the drugs to prevent angiogenesis. Many previous reviews on pathogenesis on AD have explained neuronal degeneration, but this review focuses on the effect of angiogenesis on the pathology of AD, which is believed to be the root cause for neuronal degeneration. This review attempts to launch a relation between vascular damage and AD pathology. If AD is anangiogenes is-related condition, then antiangiogenic drugs aiming at the abnormal cerebral EC will stop and treat the disease. Also, treating the disease from the root cause decreases the side effects of treatment.