Abstract
This article sets out a case for considering generally available polyvalent vaccines such as BCG, MMR and DPT to be repurposed for treating emerging cognitive decline in elderly people through reducing neuroinflammation via microglial activation. Up to now, treatments to reduce parenchymal oligomers such as Amyloid beta in Alzheimer’s disease have been clinically unsuccessful. Therefore, an alternative approach to try and directly attenuate microglial activation has utility.
Highlights
This article sets out a case for considering generally available polyvalent vaccines such as Bacillus Calmette-Guérin (BCG), MMR and DPT to be repurposed for treating emerging cognitive decline in elderly people through reducing neuroinflammation via microglial activation
Microglial activation can be measured via Positron Emission Tomography (PET) using radioactive ligands binding to benzodiazepine receptors [2]
Precipitants of microglial activation, studies in mice show that rapidly replicating neurones produce a signalling protein call fractalkine, which binds to the microglial receptor CX3CR1, causing activation [6]
Summary
Microglia are the scavenger cells in the brain, with multiple roles of phagocytosing cell debris, viral particles and unused synaptic dendritic spines [1]. Microglial activation is not a single pathway; there are 2 pathways quiescent microglia can proceed to in the face of pathogens (like viral particles) or when presented with neuronal damage (for example following traumatic brain injury). Activation cells can provide a neuroprotective effect [4] These 2 phenotypes are mutually inhibitory; similar to the peripheral T helper cells proceeding to either TH1 (inflammatory and cytotoxic) or TH2 (antibody producing) cell lines [5]. The relationship between stress and microglial activation is based on the release of cytokines such as IL6. This cytokine penetrates the blood brain barrier and activates microglia in the central nervous system and plays a key role in the pathogenesis of mood disorders [8]. By Interleukin 4 or Interleukin 13 to an M2 phenotype for resolution of inflammation and tissue repair [10]
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