Glucose Metabolism, Neural Cell Senescence and Alzheimer's Disease.
Qianqian WangLinyan DuanXingfan LiYifu WangWenna GuoFangxia GuanShanshan MaPublished in: International journal of molecular sciences (2022)
Alzheimer's disease (AD), an elderly neurodegenerative disorder with a high incidence and progressive memory decline, is one of the most expensive, lethal, and burdening diseases. To date, the pathogenesis of AD has not been fully illustrated. Emerging studies have revealed that cellular senescence and abnormal glucose metabolism in the brain are the early hallmarks of AD. Moreover, cellular senescence and glucose metabolism disturbance in the brain of AD patients may precede amyloid-β deposition or Tau protein phosphorylation. Thus, metabolic reprogramming targeting senescent microglia and astrocytes may be a novel strategy for AD intervention and treatment. Here, we recapitulate the relationships between neural cell senescence and abnormal glucose metabolism (e.g., insulin signaling, glucose and lactate metabolism) in AD. We then discuss the potential perspective of metabolic reprogramming towards an AD intervention, providing a theoretical basis for the further exploration of the pathogenesis of and therapeutic approach toward AD.
Keyphrases
- dna damage
- endothelial cells
- single cell
- type diabetes
- multiple sclerosis
- stress induced
- newly diagnosed
- end stage renal disease
- ejection fraction
- cognitive decline
- risk factors
- inflammatory response
- working memory
- oxidative stress
- cerebrospinal fluid
- blood pressure
- insulin resistance
- neuropathic pain
- middle aged
- drug delivery
- prognostic factors
- spinal cord injury
- skeletal muscle
- mesenchymal stem cells
- binding protein
- blood brain barrier
- brain injury
- smoking cessation
- risk assessment