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by hiren58
Last updated 6 years ago

Cell Biology

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Such A-β neurons were associated with astroglial activation (pre-plaque), likely triggered by the release of inflammatory markers as a stress reaction to the burden of A-β; microglial activation around the hippocampus prior to plaque deposition, triggered by accumulation of A-β especially in the subiculum. Furthermore, they found that fractalkine (chemokine) levels increased from the pre to post-plaque stages, implicating it in the activation/recruitment of the glia. They hypothesized that targeting this pathway early on, could help by prohibiting the glial activity, which coincides with the early cognitive impairments in AD.

Using a transgenic rat model, McGill-R-Thy1-APP (pre and post-plaque deposition/6 and 13 months) that mimicked human AD pathologies, Hanzel et al. found that there was an increase in the classical inflammatory markers such as the cytokine IL-1β prior to plaque deposition, at around 4-6 months of age, especially in the vicinity of A-β-burdened neurons, strongly suggesting that there is an early inflammatory response.

Neuronal driven pre-plaque inflammation in a transgenic rat model of Alzheimer's disease


Silent Pathology

A-β burdened neurons

Alzheimer's Disease

The characteristic pathologies experienced in Alzheimer's disease (AD) can be divided into the extracellular amyloid (A-β) plaques and intracellular neurofibrillary tangles due to abnormally phosphorylated protein tau. With amyloid plaques comes inflammation of the brain, although it is not clear if the A-β can cause an early inflammatory response. Hanzel et al. looked at whether this pro-inflammatory response was present before the A-β plaque deposition because the onset of AD could be potentially blocked or delayed by inhibiting the response, which could then be thought of as a silent pathology for AD.

Pre-plaque inflammation


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