Microglial lactate metabolism as a potential therapeutic target for Alzheimer's disease

Sustained activation of glycolytic metabolism would lead to low efficiency of ATP production and compromise of microglial immune functions [9]. Since the energy metabolism is required for Aβ phagocytosis and clearance, the low efficiency of ATP production due to glycolytic metabolism would impair th...

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Bibliographic Details
Published in:Molecular neurodegeneration 2022-05, Vol.17 (1), p.36-36, Article 36
Main Authors: Zhao, Yingjun, Xu, Huaxi
Format: Article
Language:English
Subjects:
Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Brain - metabolism
Energy metabolism
Epigenetics
Feedback
Gene expression
Glucose
Glucose metabolism
Glycolysis
Histone H4
Humans
Immune clearance
Inflammation
Lactates - metabolism
Lactic acid
Lysine
Metabolic disorders
Microglia
Microglia - metabolism
Neurodegenerative diseases
Parkinson's disease
Pathogenesis
Phagocytes
Phagocytosis
Phosphorylation
Research Highlight
Therapeutic targets
Trends
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Summary:Sustained activation of glycolytic metabolism would lead to low efficiency of ATP production and compromise of microglial immune functions [9]. Since the energy metabolism is required for Aβ phagocytosis and clearance, the low efficiency of ATP production due to glycolytic metabolism would impair the phagocytic function of microglia and result in Aβ accumulation. In summary, this study highlights a crosstalk between lactate metabolism and histone lactylation in microglia, and reveals how this lactate-derived epigenetic modification exacerbates microglial dysfunction and neuroinflammation in the development and progression of AD. [...]targeting lactate metabolism disorder may represent a novel strategy for AD intervention (Fig. 1). Positive feedback regulation of microglial glucose metabolism by histone H4 lysine 12 lactylation in Alzheimer's disease.
ISSN:1750-1326
1750-1326
DOI:10.1186/s13024-022-00541-z