Acta Neuropathologica

, Volume 129, Issue 5, pp 763–766 | Cite as

Does the difference between PART and Alzheimer’s disease lie in the age-related changes in cerebral arteries that trigger the accumulation of Aβ and propagation of tau?

  • Roy O. WellerEmail author
  • Cheryl A. Hawkes
  • Roxana O. Carare
  • John Hardy


Primary age-related tauopathy (PART) [7] is characterised by a limited distribution of tau pathology, compared with Alzheimer’s disease (AD), and an absence of amyloid-β (Aβ) plaques. Clinically, patients with PART are older and only a minority have profound cognitive impairment. Neurofibrillary tangles (NFTs) containing hyperphosphorylated tau spread in an age-related manner from brainstem to cerebral cortical areas [3] and the presence of Aβ plaques is associated with acceleration in the propagation of NFTs in the pathogenesis of AD [11, 18]. The amyloid cascade [8] appears to drive the hyperphosphorylation and propagation of tau [6, 16] and Aβ oligomers have a toxic effect upon synapses [16].

In the context of PART, we ask the question “Why is there relatively limited spread of NFTs and few if any Aβ plaques in PART compared with AD?” In order to answer these questions, we examine evidence that ageing of cerebral arteries is a trigger for the amyloid cascade and...


Cerebral Artery Cerebral Amyloid Angiopathy Artery Wall Tauopathy Extracranial Internal Carotid Artery 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Springer-Verlag Berlin Heidelberg 2015

Authors and Affiliations

  • Roy O. Weller
    • 1
    Email author
  • Cheryl A. Hawkes
    • 2
  • Roxana O. Carare
    • 1
  • John Hardy
    • 3
  1. 1.Neuropathology, Clinical and Experimental Sciences, Faculty of Medicine, Institute for Life Sciences, Southampton University HospitalUniversity of SouthamptonSouthamptonUK
  2. 2.Department of Life, Health and Chemical Sciences, Faculty of ScienceOpen UniversityMilton KeynesUK
  3. 3.Reta Lila Research Laboratories and Department of Molecular NeuroscienceUCL Institute of NeurologyLondonUK

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