Diagram showing Hippocampus, an area affected by Alzheimer’s Disease (credits Appendix A)
Crary and colleagues have written this 2014 paper on PART (Primary Age Related Tauopathy) (see also this paper by Crary). I’ve highlighted a few key points about the hypothesis from this paper
(1) The PART hypothesis is driven by pathological findings
(2) PART distinguishes between pathology and clinical manifestation
(3) Comorbid pathology presents a challenge when identifying ‘pure’ clinical correlates of PART
(4) Ambiguity in the hypothesis. PART has been described as:
(a) Distinct from Alzheimer’s Disease
(b) A subset of Alzheimer’s Disease cases
(c) An early stage of Alzheimer’s Disease (i.e. the Amyloid plaques may be expected to follow the appearance of the tangles)
(d) On a continuum with Alzheimer’s Disease
(5) PART also maps onto the pathology associated with several previous descriptors
(a) ‘Tangle Predominant Senile Dementia’
(b) ‘Tangle only Dementia’
(c) ‘Preferential Development of NFT without senile plaques’
(d) ‘Senile Dementia of the Neurofibrillary Tangle Type’
(6) TPSD (5a above) has previously been classed as a Frontotemporal Lobar Degeneration
The reader can see from the above that there are many possible variations of the hypothesis.
Appendix A – Credits
Picture by FG Designs. Creative Commons License.
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[…] at alternatives to the Amyloid Cascade hypothesis in this post. There was a discussion of the PART hypothesis which was driven by histopathological findings. There was also a look at Small and Duff’s […]
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[…] at alternatives to the Amyloid Cascade hypothesis in this post. There was a discussion of the PART hypothesis which was driven by histopathological findings. There was also a look at Small and Duff’s […]
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