Title:A Systematic Review of Updated Mechanistic Insights Towards
Alzheimer’s Disease
Volume: 22
Issue: 8
Author(s): Arun Mittal*, Rupali Sharma, Satish Sardana, Parveen Kumar Goyal, Mona Piplani and Anima Pandey
Affiliation:
- Amity Institute of Pharmacy, Amity University Haryana, Manesar, Gurgaon, Haryana-122413, India
Keywords:
CNS, TREMZ, alzheimer, neurofibrillary tangles, amyloid β, lysosomal membrane.
Abstract:
Background: Alzheimer's disease (AD) is a degenerative neurological disorder that impairs
memory, cognitive abilities, and the ability to do everyday activities. This neurodegenerative disease is
growing increasingly common as the world's population ages. Here, we reviewed some of the key findings
showing the function of Aβ peptide, oxidative stress, free radical damage Triggering Receptors Expressed
cn Myeloid Cells 2 (TREM2), Nitric Oxide (NO) and gut microbiota in the aetiology of AD.
Methods: The potentially relevant online medical databases, namely PubMed, Scopus, Google Scholar,
Cochrane Library, and JSTOR, were exhaustively researched. In addition, the data reported in the
present study were primarily intervened on the basis of the timeline selected from 1 January 2000 to 31
October 2021. The whole framework was designed substantially based on key terms and studies selected
by virtue of their relevance to our investigations.
Results: Findings suggested that channels of free radicals, such as transition metal accumulation and
genetic factors, are mainly accountable for the redox imbalance that assist to understand better the
pathogenesis of AD and incorporating new therapeutic approaches. Moreover, TREM2 might elicit a
protective function for microglia in AD. NO causes an increase in oxidative stress and mitochondrial
damage, compromising cellular integrity and viability. The study also explored that the gut and CNS
communicate with one another and that regulating gut commensal flora might be a viable therapeutic
for neurodegenerative illnesses like AD.
Conclusion: There are presently no viable therapies for Alzheimer's disease, but recent breakthroughs in
our knowledge of the disease's pathophysiology may aid in the discovery of prospective therapeutic targets.
