Abstract
Rationale: Energy metabolism disorder is a widespread feature that exists in the early clinical stages of Alzheimer’s disease (AD). Astrocyte is the most numerous and the largest glial cell in the brain. By transporting energetic fuels such as lactate and ketones to neurons, astrocytes play a pivotal role in maintaining the cerebral energy homeostasis. Sodium butyrate (NaB), a type of short-chain fatty acid; its anti-inflammatory effect; and inhibition on histone deacetylases have been widely studied.
Methods: Spatial memory and cognitive ability of mice were assessed by using behavioral tests. Western blotting and ELISA kits were used to detect related protein levels and other biochemical markers, respectively.
Objectives: To prove the therapeutic effect of NaB on AD cognitive impairment and provide possible research ideas for mechanism exploration.
Results: Administration of NaB could improve the cognitive impairments induced by Aβ25-35 in mice. Furthermore, NaB could promote the differentiation of astrocytes towards A2-neuron-protective subtype, astroglial mitochondrial function, and lactate shuttle between astrocytes and neurons.
Conclusion: These findings reveal the effect of sodium butyrate on astrocytes, which may improve the pathological status of AD and provide experimental basis for sodium butyrate treatment of AD.
PMID: 34812899 DOI: 10.1007/s00213-021-06025-0
