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Alzheimer's disease: Innate immunity gone awry?

Theodore B VanItallie1

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Occult neuroinflammation contributes to Alzheimer's disease (AD) progression. Ketone esters, like beta-hydroxybutyrate (βOHB), show preclinical promise in protecting the brain and warrant clinical investigation for AD treatment.

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Area of Science:

  • Neuroscience
  • Immunology
  • Biochemistry

Background:

  • Neuroinflammation, often subtle, is implicated in Alzheimer's disease (AD) pathogenesis and progression.
  • A compromised blood-brain barrier (BBB) is observed in early AD, potentially initiating and exacerbating the disease.
  • Amyloid-beta burden correlates poorly with cognitive decline in AD; synapse loss correlates better, with oligomeric forms (oAβs) being particularly synaptotoxic.

Purpose of the Study:

  • To explore the role of neuroinflammation and the blood-brain barrier in Alzheimer's disease.
  • To investigate the potential neuroprotective effects of beta-hydroxybutyrate (βOHB) against inflammasome activation and histone deacetylation.
  • To highlight the need for clinical trials evaluating oral βOHB preparations for Alzheimer's disease.

Main Methods:

  • Review of existing literature on neuroinflammation, Alzheimer's disease biomarkers, and the effects of βOHB.
  • Analysis of studies linking amyloid-beta, microglia activation, and cognitive decline.
  • Examination of preclinical data on βOHB's impact on NLRP3 inflammasome and histone deacetylation.

Main Results:

  • Occult neuroinflammation and BBB dysfunction are key factors in AD.
  • Oligomeric amyloid-beta (oAβs) cause synaptic toxicity, contributing to early memory loss.
  • Preclinical studies suggest βOHB may mitigate neuroinflammation by inhibiting the NLRP3 inflammasome and histone deacetylation.

Conclusions:

  • Neuroinflammation and BBB leakage are critical in AD development and progression.
  • βOHB demonstrates potential neuroprotective effects against key pathological pathways in AD.
  • Clinical trials are necessary to confirm the therapeutic efficacy of oral βOHB in human subjects with Alzheimer's disease.