| Home > Publications Database > PART is part of Alzheimer disease. |
| Journal Article | DZNE-2020-04206 |
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2015
Springer
Heidelberg
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Please use a persistent id in citations: doi:10.1007/s00401-015-1390-7
Abstract: It has been proposed that tau aggregation confined to entorhinal cortex and hippocampus, with no or only minimal Aβ deposition, should be considered as a 'primary age-related tauopathy' (PART) that is not integral to the continuum of sporadic Alzheimer disease (AD). Here, we examine the evidence that PART has a pathogenic mechanism and a prognosis which differ from those of AD. We contend that no specific property of the entorhinal-hippocampal tau pathology makes it possible to predict either a limited progression or the development of AD, and that biochemical differences await an evidence base. On the other hand, entorhinal-hippocampal tau pathology is an invariant feature of AD and is always associated with its development. Rather than creating a separate disease entity, we recommend the continued use of an analytical approach based on NFT stages and Aβ phases with no inference about hypothetical disease processes.
Keyword(s): Aging: pathology (MeSH) ; Alzheimer Disease: diagnosis (MeSH) ; Alzheimer Disease: metabolism (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Amyloid beta-Peptides: metabolism (MeSH) ; Diagnosis, Differential (MeSH) ; Disease Progression (MeSH) ; Entorhinal Cortex: pathology (MeSH) ; Hippocampus: pathology (MeSH) ; Humans (MeSH) ; Tauopathies: diagnosis (MeSH) ; Tauopathies: metabolism (MeSH) ; Tauopathies: pathology (MeSH) ; tau Proteins: metabolism (MeSH) ; Amyloid beta-Peptides ; tau Proteins
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