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- Title
Neurotoxic b-amyloid oligomers cause mitochondrial dysfunction--the trigger for PANoptosis in neurons.
- Authors
Xiangyuan Meng; Qi Song; Zinan Liu; Xinpeng Liu; Yujie Wang Jinyu Liu
- Abstract
As the global population ages, the incidence of elderly patients with dementia, represented by Alzheimer's disease (AD), will continue to increase. Previous studies have suggested that b-amyloid protein (Ab) deposition is a key factor leading to AD. However, the clinical efficacy of treating AD with anti-Ab protein antibodies is not satisfactory, suggesting that Ab amyloidosis may be a pathological change rather than a key factor leading to AD. Identification of the causes of AD and development of corresponding prevention and treatment strategies is an important goal of current research. Following the discovery of soluble oligomeric forms of Ab (AbO) in 1998, scientists began to focus on the neurotoxicity of AbOs. As an endogenous neurotoxin, the active growth of AbOs can lead to neuronal death, which is believed to occur before plaque formation, suggesting that AbOs are the key factors leading to AD. PANoptosis, a newly proposed concept of cell death that includes known modes of pyroptosis, apoptosis, and necroptosis, is a form of cell death regulated by the PANoptosome complex. Neuronal survival depends on proper mitochondrial function. Under conditions of AbO interference, mitochondrial dysfunction occurs, releasing lethal contents as potential upstream
- Subjects
ENDOCYTOSIS; MITOCHONDRIA; ALZHEIMER'S disease; AUTOPHAGY; APOPTOSIS; ENERGY metabolism; CELL death; AMYLOID beta-protein precursor; DISEASE progression
- Publication
Frontiers in Aging Neuroscience, 2024, p1
- ISSN
1663-4365
- Publication type
Article
- DOI
10.3389/fnagi.2024.1400544