Alzheimer's disease (AD) is a neurodegenerative disease distinguished by memory impairment and dementia. Amyloid beta (Aβ), a peptide, that recreates an influential role in neuronal damage by proliferation in the brain (plaque) and cerebral amyloid angiopathy (CAA).It is also caused by neurodegeneration due to the loss of acetylcholine). Aβ is produced via consecutive Amyloidprotein precursor (APP) divisions by the β and γ secretase, both found in lipid rafts. The modulation of these components is a critical element in Aβ generation during AD development. Aβ derived from Amyloid precursor protein (APP) is misfolded, and deposits as a plaque in the brain, thought to be a characteristic of AD. Aβ deposition in the brain originates from the brain itself. However, circulating Aβ can also cross the blood-brain barrier through the influence of both, contributing to AD-type pathologies. Aβ aggregation and clearance become an operational analysis area for healing and controlling AD. Therefore, this feature article intends to provide details of the aggregation mechanism and physiological role of Aβ peptide.