Volume - 13 | Issue-1
Volume - 13 | Issue-1
Volume - 13 | Issue-1
Volume - 13 | Issue-1
Volume - 13 | Issue-1
Alzheimer's disease is one of the most prevalent age-linked neurodegenerative conditions afflicting older people. (AD).1,2 The main risk factor for the development and worsening of AD is age, and the risk almost doubles every five years in adults over 65. 3–5 Over 4.4 crores of people were thought to be affected by this neurological condition in 2015, according to estimates. Nonetheless, it is anticipated that by 2050, this number would have doubled.6,7 A complicated illness that is genetically predisposed and ecofriendly variables play a substantial role in the pathology, it is revealed that the majority of AD patients (over 95%) either SAD (sporadic AD) or LOAD (late-onset AD).8,9 On the other side, familial AD or earlyonset AD (EOAD) are only detected in less than 5% of AD patients (FAD). It has been discovered that mutations in either of the presenilin-1 (PSEN1), presenilin-2 (PSEN2), and amyloid precursor protein (APP) genes could induce the aforementioned forms of AD (i.e., EOAD and FAD).