Inverse association of Pin1 and tau accumulation in Alzheimer's disease hippocampus

Clicks: 122
ID: 116481
1970
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #343 of 438 articles by views in acta neuropathologica

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 438 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Neurofibrillary degeneration, one of the pathological hallmarks of Alzheimer's disease, is not ubiquitous to all brain regions or neurons. While a high degree of vulnerability has been documented for entorhinal cortex, hippocampal and neocortical pyramidal neurons other brain structures are largely spared. Even within highly vulnerable regions such as hippocampus neurons are affected to a variable extent. The molecular basis for this selective susceptibility remains unknown. Neurofibrillary degeneration involves hyperphosphorylation of tau which critically impairs its binding capacity to microtubule and, therefore, is believed to disrupt the axonal cytoskeleton. Recently, Lu et al. [Nature (1999) 399:784] described the ability of the peptidyl-prolyl cis-trans isomerase Pin1 to recover microtubule-binding affinity and microtubule stabilisation of phosphorylated tau. In the present study, we analysed the potential involvement of Pin1 in selective vulnerability of hippocampal neurons to neurofibrillary degeneration in Alzheimer's disease. Pin1 immunoreactivity appeared as cytoplasmic granules affecting hippocampal subfields to a different extent (CA2>subiculum>CA1>CA3/CA4). Since the main markers of granulovacuolar degeneration do not co-label Pin1-immunoreactive granules, we propose that these granules may represent a new lesion in Alzheimer's disease. Neurons containing Pin1 granules were devoid of neurofibrillary tangles. Granular accumulation of Pin1 may correspond to an absence of neurofibrillary lesions in these cells and might be associated with other mechanisms of neuronal degeneration.
Reference Key
holzer1970actainverse Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Max Holzer;Ulrich Gärtner;Andrea Stöbe;Wolfgang Härtig;Hildegard Gruschka;Martina K. Brückner;Thomas Arendt;Max Holzer;Ulrich Gärtner;Andrea Stöbe;Wolfgang Härtig;Hildegard Gruschka;Martina K. Brückner;Thomas Arendt;
Journal acta neuropathologica
Year 1970
DOI
doi:10.1007/s00401-002-0581-1
URL
https://link.springer.com/article/10.1007/s00401-002-0581-1
Keywords
pathology neurosciences

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.