Journal
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
Volume 1868, Issue 6, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.bbamcr.2021.118997
Keywords
Bcl-2; Calcium; Neurons; Mitochondria; Apoptosis; Alzheimer's disease
Categories
Funding
- Research Foundation - Flanders (FWO) [G.0634.13N, G.0C91.14N, G.0A34.16N, G090118N, G0E7520N, S006617N, G078117N, G056017N, G0C4220N]
- Research Council - KU Leuven [OT14/101, C14/19/101, AKUL/19/34, C16/15/073]
- Central European Leuven Strategic Alliance [CELSA/18/040]
- Stichting Alzheimer Onderzoek (SAO-FRA) [2020-0030]
- National Institutes of Health [R01AG055577]
- Russian Science Foundation [20-45-01004]
- Eye Hope Foundation/Koning Boudewijnstichting [2020-J1160630214966]
- Stichting Alzheimer Onderzoek (SAO IP3 RECEPTOR)
- VIB
- Russian Science Foundation [20-45-01004] Funding Source: Russian Science Foundation
Ask authors/readers for more resources
The Bcl-2 protein family plays crucial roles in cellular health and neuronal function, with involvement in regulating apoptosis and Ca2+ signaling. Dysregulation of Bcl-2 proteins may contribute to the progression of neurodegenerative diseases like Alzheimer's, suggesting a potential therapeutic target in the treatment of AD.
The family of B-cell lymphoma-2 (Bcl-2) proteins exerts key functions in cellular health. Bcl-2 primarily acts in mitochondria where it controls the initiation of apoptosis. However, during the last decades, it has become clear that this family of proteins is also involved in controlling intracellular Ca2+ signaling, a critical process for the function of most cell types, including neurons. Several anti- and pro-apoptotic Bcl-2 family members are expressed in neurons and impact neuronal function. Importantly, expression levels of neuronal Bcl-2 proteins are affected by age. In this review, we focus on the emerging roles of Bcl-2 proteins in neuronal cells. Specifically, we discuss how their dysregulation contributes to the onset, development, and progression of neurodegeneration in the context of Alzheimer's disease (AD). Aberrant Ca2+ signaling plays an important role in the pathogenesis of AD, and we propose that dysregulation of the Bcl-2-Ca2+ signaling axis may contribute to the progression of AD and that herein, Bcl-2 may constitute a potential therapeutic target for the treatment of AD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available