Genetic and non-genetic factors responsible for mitochondrial failure and Alzheimer’s disease

Gao, Kuo; Niu, Meiying; Zhai, Xing; Huang, Youliang; Tian, Xin; Li, Tiangang

doi:10.2298/gensr1402631g

Cited by 2 publications

(2 citation statements)

References 129 publications

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“…Moreover, the central nervous system's early embryonic processes and neuronal stem cell growth can be mediated by sAPPα [63]. In response to specific neuroprotective agents, it has been proposed that sAPPα could suppress cyclin-dependent kinase 5 (CDK5) activation induced by excitotoxicity and take part in diverse excitoprotective mechanisms [64]. Notably, in APP-deficient mice, sAPPα expression alone is sufficient to reverse defects, indicating that sAPPα might facilitate most APP functioning.…”

Section: Amyloid β Hypothesismentioning

confidence: 99%

An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer’s Disease

Ratan,

Rajput,

Maleysm

et al. 2023

Biomedicines

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Alzheimer’s disease (AD) is the most prominent neurodegenerative disorder in the aging population. It is characterized by cognitive decline, gradual neurodegeneration, and the development of amyloid-β (Aβ)-plaques and neurofibrillary tangles, which constitute hyperphosphorylated tau. The early stages of neurodegeneration in AD include the loss of neurons, followed by synaptic impairment. Since the discovery of AD, substantial factual research has surfaced that outlines the disease’s causes, molecular mechanisms, and prospective therapeutics, but a successful cure for the disease has not yet been discovered. This may be attributed to the complicated pathogenesis of AD, the absence of a well-defined molecular mechanism, and the constrained diagnostic resources and treatment options. To address the aforementioned challenges, extensive disease modeling is essential to fully comprehend the underlying mechanisms of AD, making it easier to design and develop effective treatment strategies. Emerging evidence over the past few decades supports the critical role of Aβ and tau in AD pathogenesis and the participation of glial cells in different molecular and cellular pathways. This review extensively discusses the current understanding concerning Aβ- and tau-associated molecular mechanisms and glial dysfunction in AD. Moreover, the critical risk factors associated with AD including genetics, aging, environmental variables, lifestyle habits, medical conditions, viral/bacterial infections, and psychiatric factors have been summarized. The present study will entice researchers to more thoroughly comprehend and explore the current status of the molecular mechanism of AD, which may assist in AD drug development in the forthcoming era.

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Section: Amyloid β Hypothesismentioning

confidence: 99%

An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer’s Disease

Ratan,

Rajput,

Maleysm

et al. 2023

Biomedicines

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“…Mutations in three genes have been identified as causative factors for familial AD, including the amyloid precursor protein ( APP ) gene (chr 21), the presenilin 1 ( PSEN1 ) gene (chr14), and presenilin 2 ( PSEN2 ) (chr1) [ 4 , 5 , 6 , 7 , 8 ]. The most common genetic risk factor for AD in Caucasian groups, including the Russian population, is a polymorphism in apolipoprotein E ( APOE ) (chr19) [ 9 , 10 , 11 , 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Neuronal Hyperactivation in EEG Data during Cognitive Tasks Is Related to the Apolipoprotein J/Clusterin Genotype in Nondemented Adults

Пономарева

Andreeva

Protasova

et al. 2023

IJMS

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The clusterin (CLU) rs11136000 CC genotype is a probable risk factor for Alzheimer’s disease (AD). CLU, also known as the apolipoprotein J gene, shares certain properties with the apolipoprotein E (APOE) gene with a well-established relationship with AD. This study aimed to determine whether the electrophysiological patterns of brain activation during the letter fluency task (LFT) depend on CLU genotypes in adults without dementia. Previous studies have shown that LFT performance involves activation of the frontal cortex. We examined EEG alpha1 and alpha2 band desynchronization in the frontal regions during the LFT in 94 nondemented individuals stratified by CLU (rs11136000) genotype. Starting at 30 years of age, CLU CC carriers exhibited more pronounced task-related alpha2 desynchronization than CLU CT&TT carriers in the absence of any differences in LFT performance. In CLU CC carriers, alpha2 desynchronization was significantly correlated with age. Increased task-related activation in individuals at genetic risk for AD may reflect greater “effort” to perform the task and/or neuronal hyperexcitability. The results show that the CLU genotype is associated with neuronal hyperactivation in the frontal cortex during cognitive tasks performances in nondemented individuals, suggesting systematic vulnerability of LFT related cognitive networks in people carrying unfavorable CLU alleles.

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Genetic and non-genetic factors responsible for mitochondrial failure and Alzheimer’s disease

Cited by 2 publications

References 129 publications

An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer’s Disease

An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer’s Disease

Neuronal Hyperactivation in EEG Data during Cognitive Tasks Is Related to the Apolipoprotein J/Clusterin Genotype in Nondemented Adults

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