An Infection Hypothesis to Explain the Amyloid Hypothesis of Alzheimer's Disease
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15

Aug

2018

15

Aug

2018

An Infection Hypothesis to Explain the Amyloid Hypothesis of Alzheimer’s Disease

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Theory and evidence for persistent infection as a cause of Alzheimer’s disease continues to grow in scope and plausibility. In general this supports rather than replaces past thinking on amyloid-β and its role in the development of Alzheimer’s. It provides an explanation as to why it is that levels of amyloid-β rise over time to produce the early disruptions and changes in the biochemistry of the brain that are necessary for later neurodegeneration to take place. Other compelling lines of work provide evidence for entirely separate mechanisms by which levels of amyloid-β can grow in later life, such as declining drainage of cerebrospinal fluid. It seems plausible that all may be correct to some degree, and that many of these proposed processes are significant, each adding their own contribution to the progressive decline of the brain.

Alzheimer’s disease (AD) is the most frequent type of dementia. The pathological hallmarks of the disease are extracellular senile plaques composed of beta-amyloid peptide (Aβ) and intracellular neurofibrillary tangles composed of phosphorylated tau (pTau). These findings led to the “beta-amyloid hypothesis” that proposes that Aβ

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