Revisiting the focal role of endostatin and environmental factors in Alzheimer's disease.

Autor: Behl T; Amity School of Pharmaceutical Sciences, Amity University, Mohali, Punjab, India., Dahim MA; Department of Civil Engineering, King Khalid University, Guraiger, Abha, 62529, Kingdom of Saudi Arabia., Aleya L; Laboratoire de Chrono-Environnement, UMR CNRS 6249, Université de Bourgogne Franche-Comté, La Bouloie, 25030, Besancon Cedex, France. lotfi.aleya@univ-fcomte.fr.
Jazyk: angličtina
Zdroj: Environmental science and pollution research international [Environ Sci Pollut Res Int] 2024 Jul; Vol. 31 (32), pp. 44511-44517. Date of Electronic Publication: 2024 Jun 29.
DOI: 10.1007/s11356-024-34113-z
Abstrakt: Alzheimer's disease (AD) is a condition initiated by the assimilation of β-amyloid plaques (Aβ) and tau tangles, leading to neurodegeneration. It involves frequently cognitive decline as well as memory impairment in patients. Efforts in therapeutic interventions are currently facing challenges in identifying targets within this scaffold that can significantly alter the clinical course for individuals with AD. Moreover, in AD, neurons release a protein called endostatin, which accumulates in Aβ plaques and enhances AD. This accumulation of Aβ in the triggers a cascade of events leading to synaptic dysfunction, neuroinflammation, and ultimately neuronal death. Environmental factors nowadays increase the risk of AD with prolonged exposure of heavy metals such as copper (Cu), lead (Pb), mercury (Hg), cadmium (Cd), and other pesticides. It has been observed that these factors can cause the aggregation of Aβ and tau which initiates the plaque formation and hence leads to enhanced pathogenesis of AD. This review summarizes the interlinking between heavy metals, environmental factors, pesticides, endostatin, and progression of AD has been deliberated with recent findings.
(© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)
Databáze: MEDLINE
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