Summary of
D-β-Hydroxybutyrate Protects Neurons in Models of Alzheimer’s and Parkinson’s Disease
By
Purpose
To evaluate whether the ketone body D-β-hydroxybutyrate can protect neurons from neurotoxins associated with Alzheimer’s and Parkinson’s diseases.
Methods
Researchers exposed cultured rat mesencephalic neurons and hippocampal neurons to either MPP+ (a dopaminergic neurotoxin) or Aβ1–42 (amyloid beta fragment). Parallel cultures received 4 mM D-BHB. Cell viability, neurite outgrowth, and oxidative damage were assessed over 36 hours.
Results
BHB significantly protected dopaminergic neurons from MPP+ toxicity and hippocampal neurons from Aβ1–42 toxicity. In both models, BHB restored neurite outgrowth, improved cell survival, and enhanced metabolic resilience. Mechanistically, BHB bypassed mitochondrial PDH blockades, reduced oxidative stress by oxidizing coenzyme Q, and restored TCA cycle function.
Conclusion
BHB offers broad neuroprotection by improving mitochondrial efficiency and reducing oxidative damage in models of Alzheimer’s and Parkinson’s. These results support ketone therapy as a potential tool for addressing common metabolic deficiencies found in age-related neurodegeneration.
