Metabolic disorder in Alzheimer’s disease

Poddar, Mrinal K.; Banerjee, Subrata; Chakraborty, Apala; Dutta, Debasmita

doi:10.1007/s11011-021-00673-z

Cited by 25 publications

(9 citation statements)

References 274 publications

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“…In the early pathological state of AD, glucose utilization (up to 45%) is reduced, which is closely related to the alteration of insulin signaling. It has been reported that poor glucose utilization and insulin resistance can enhance Aβ deposition and decrease its clearance ( 60 ). Besides, brains with AD have been found to have a higher incidence of abnormal lipid metabolism, which is the early risk factor for the development of amyloid pathology ( 61 ).…”

Section: Pathogenesis Of Admentioning

confidence: 99%

The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer’s disease

Meng

et al. 2022

Front. Endocrinol.

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Since type 2 diabetes mellitus (T2DM) is a risk factor for Alzheimer’s disease (AD) and both have the same pathogenesis (e.g., insulin resistance), drugs used to treat T2DM have been gradually found to reduce the progression of AD in AD models. Of these drugs, glucagon-like peptide 1 receptor (GLP-1R) agonists are more effective and have fewer side effects. GLP-1R agonists have reducing neuroinflammation and oxidative stress, neurotrophic effects, decreasing Aβ deposition and tau hyperphosphorylation in AD models, which may be a potential drug for the treatment of AD. However, this needs to be verified by further clinical trials. This study aims to summarize the current information on the mechanisms and effects of GLP-1R agonists in AD.

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Section: Pathogenesis Of Admentioning

confidence: 99%

The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer’s disease

Meng

et al. 2022

Front. Endocrinol.

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“…[37] Altered insulin signaling in the brain promotes tau cleavage and restricts alternative splicing of tau. [38][39][40] A number of energy-related enzymes, which play an important role in the function of the TCA cycle, are dysregulated in AD. The dysfunction of the AMPK signaling pathway may be involved in AD as AMPK is a key sensor and regulator of energy metabolism.…”

Section: Neuronmentioning

confidence: 99%

Aberrant energy metabolism in Alzheimer’s disease

Jin

et al. 2022

Journal of Translational Internal Medicine

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To maintain energy supply to the brain, a direct energy source called adenosine triphosphate (ATP) is produced by oxidative phosphorylation and aerobic glycolysis of glucose in the mitochondria and cytoplasm. Brain glucose metabolism is reduced in many neurodegenerative diseases, including Alzheimer’s disease (AD), where it appears presymptomatically in a progressive and region-specific manner. Following dysregulation of energy metabolism in AD, many cellular repair/regenerative processes are activated to conserve the energy required for cell viability. Glucose metabolism plays an important role in the pathology of AD and is closely associated with the tricarboxylic acid cycle, type 2 diabetes mellitus, and insulin resistance. The glucose intake in neurons is from endothelial cells, astrocytes, and microglia. Damage to neurocentric glucose also damages the energy transport systems in AD. Gut microbiota is necessary to modulate bidirectional communication between the gastrointestinal tract and brain. Gut microbiota may influence the process of AD by regulating the immune system and maintaining the integrity of the intestinal barrier. Furthermore, some therapeutic strategies have shown promising therapeutic effects in the treatment of AD at different stages, including the use of antidiabetic drugs, rescuing mitochondrial dysfunction, and epigenetic and dietary intervention. This review discusses the underlying mechanisms of alterations in energy metabolism in AD and provides potential therapeutic strategies in the treatment of AD.

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“…The strongest risk factor of dementia and AD is age and lifetime cumulative multiple risk factors like genetic susceptibility, environmental exposure, and biological factors etc. are also needed to be considered for identification of preventive measures [113,114]. For example, genetic and environmental factors are responsible for Familial AD as reported by many and found to be happening in 58% of AD cases [114,115].…”

Section: Preventive Measures For Neurodegenerative Diseasesmentioning

confidence: 99%

“…are also needed to be considered for identification of preventive measures [113,114]. For example, genetic and environmental factors are responsible for Familial AD as reported by many and found to be happening in 58% of AD cases [114,115]. The involvement of APOE ε4 allele as a genetic factor as well as some other genes in AD is well established and, APOE polymorphism can partially explain the familial aggregation of AD in 15-20% of AD cases which generally affect 75 years or older patients [116,117].…”

Section: Preventive Measures For Neurodegenerative Diseasesmentioning

confidence: 99%

Oxidoreductase

2021

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His specialization includes molecular biology, biochemical pharmacology, pharmacogenetics, and biochemistry. His research fields are biochemical pharmacological studies in cancers (especially hepatic cancer), antioxidants, oxidative stress, proteasome (and its role in the treatment of hepatic cancer), experimental gastroenterology, clinical gastroenterology, and diabetes. He has published more than 60 papers in peer-reviewed journals. He received the State Encouragement award from the Scientific Research Academy, (1998). Fourteen of his students were appointed as full university professors in Egypt and Saudi Arabia.

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Metabolic disorder in Alzheimer’s disease

Cited by 25 publications

References 274 publications

The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer’s disease

The mechanism and efficacy of GLP-1 receptor agonists in the treatment of Alzheimer’s disease

Aberrant energy metabolism in Alzheimer’s disease

Oxidoreductase

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