Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)
Pathologist and Associate Professor John Crary has written an interesting piece on PART and the relationship to the Amyloid Cascade Hypothesis. PART is an acronym for Primary Age Related Tauopathy. Whilst the Amyloid Cascade Hypothesis has a great deal of supporting evidence there is data which contradicts the hypothesis.
Professor Crary references pathological findings where people with clinically diagnosed Alzheimer’s Type Dementia are found to lack evidence of Amyloid toxicity but there is the presence of tangles. He hypothesises that PART, if it is a valid construct reflects an aging mechanism in the brain independent of Amyloid plaque. He also cites evidence that the pathology is found in areas including the medial temporal lobe structures that are likely to be exposed to mechanical injury during the lifespan.
Appendix A – Credits
Picture by FG Designs. Creative Commons License.
Appendix B – Summary of the Amyloid Cascade Hypothesis
For further details see here
(1) Amyloid is central to all pathophysiological processes that lead to Alzheimer’s Disease
(2) Amyloid (including the ABeta components) is toxic
(3) An increase in Amyloid through increased production, reduced removal or both leads to increased toxicity
(4) Amyloid/ABeta leads to tangle pathophysiology
(5) Tangle pathophysiology leads to neuronal cell death
(6) Reducing Amyloid/A Beta would improve symptoms resulting from the Alzheimer’s Disease process
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