PART is part of Alzheimer disease

Acta Neuropathol. 2015 May;129(5):749-56. doi: 10.1007/s00401-015-1390-7. Epub 2015 Jan 28.


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.

MeSH terms

  • Aging / pathology*
  • Alzheimer Disease / diagnosis*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Diagnosis, Differential
  • Disease Progression
  • Entorhinal Cortex / pathology
  • Hippocampus / pathology
  • Humans
  • Tauopathies / diagnosis*
  • Tauopathies / metabolism
  • Tauopathies / pathology
  • tau Proteins / metabolism*


  • Amyloid beta-Peptides
  • tau Proteins