In a paper published in Molecular Neurodegeneration, Dr. Charles Glabe, a member of the Cure Alzheimer’s Fund Research Leadership Group, reports that treatment with the drug PLX3397 decreased the overall number of amyloid plaques in the brain and also altered the process of plaque formation. Importantly, treatment with this drug was most effective before the plaques developed. Mice that received PLX3397 performed better on a test for spatial and emotional memory but not spatial hippocampal memory. This paper discusses how a specific drug treatment could influence some specific aspects of hippocampal memory function but not others.
The paper is available open access here: https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/s13024-018-0244-x
Besides the two main classical features of amyloid beta aggregation and tau-containing neurofibrillary tangle deposition, neuroinflammation plays an important yet unclear role in the pathophysiology of Alzheimer’s disease (AD). Microglia are believed to be key mediators of neuroinflammation during AD and responsible for the regulation of brain homeostasis by balancing neurotoxicity and neuroprotective events. The authors have previously reported evidence that neuritic plaques are derived from dead neurons that have accumulated intraneuronal amyloid and further recruit Iba1-positive cells, which play a role in either neuronal demise or neuritic plaque maturation or both.
Alz Forum: “Wiping out Microglia Prevents Neuritic Plaques.” https://www.alzforum.org/news/research-news/wiping-out-microglia-prevents-neuritic-plaques
Image courtesy of the National Institute on Aging/National Institutes of Health