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Overview of a novel osmotin abolishes abnormal metabolic-associated adiponectin mechanism in Alzheimer's disease: Peripheral and CNS insightsopen access

Authors
Rehman, Inayat UrPark, Jun SungChoe, KyonghwanPark, Hyun YoungPark, Tae JuKim, Myeong Ok
Issue Date
Sep-2024
Publisher
Elsevier Ireland Ltd
Keywords
Abnormal metabolism; Adiponectin (APN); Alzheimer's disease (AD); Central nervous system (CNS); Osmotin (OSM); Periphery
Citation
Ageing Research Reviews, v.100
Indexed
SCIE
SCOPUS
Journal Title
Ageing Research Reviews
Volume
100
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/73557
DOI
10.1016/j.arr.2024.102447
ISSN
1568-1637
1872-9649
Abstract
Alzheimer's disease (AD) is a degenerative brain disease that affects millions of people worldwide. It is caused by abnormalities in cholinergic neurons, oxidative stress, and inflammatory cascades. The illness is accompanied by personality changes, memory issues, and dementia. Metabolic signaling pathways help with fundamental processes like DNA replication and RNA transcription. Being adaptable is essential for both surviving and treating illness. The body's metabolic signaling depends on adipokines, including adiponectin (APN) and other adipokines secreted by adipose tissues. Energy homeostasis is balanced by adipokines, and nutrients. Overconsumption of nutrients messes with irregular signaling of adipokines, such as APN in both peripheral and brain which leads to neurodegeneration, such as AD. Despite the failure of traditional treatments like memantine and cholinesterase inhibitors, natural plant bioactive substances like Osmotin (OSM) have been given a focus as potential therapeutics due to their antioxidant properties, better blood brain barrier (BBB) permeability, excellent cell viability, and especially nanoparticle approaches. The review highlights the published preclinical literature regarding the role of OSM in AD pathology while there is a need for more research to investigate the hidden therapeutic potential of OSM which may open a new gateway and further strengthen its healing role in the pathogenesis of neurodegeneration, especially AD. © 2024 The Authors
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