期刊
ACTA NEUROPATHOLOGICA
卷 129, 期 5, 页码 749-756出版社
SPRINGER
DOI: 10.1007/s00401-015-1390-7
关键词
Alzheimer disease; Amyloid; A beta; PART hypothesis; Tau; Tauopathy
资金
- Alzheimers Research UK [ART-PG2011-20] Funding Source: researchfish
- Medical Research Council [G0301152, MC_U105184291] Funding Source: researchfish
- Medical Research Council [G0301152, MC_U105184291] Funding Source: Medline
- MRC [G0301152, MC_U105184291] Funding Source: UKRI
It has been proposed that tau aggregation confined to entorhinal cortex and hippocampus, with no or only minimal A beta 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 A beta phases with no inference about hypothetical disease processes.
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