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Peer-reviewedCC BYAlzheimer's & dementia : the journal of the Alzheimer's Association

Structural compression and entorhinal vulnerability: Linking tentorial adjacency to tau burden and dementia progression.

  • Luyue Zhang1
  • Ana M Franceschi2
  • John F Crary3
  • Frank A Provenzano4
  • Alzheimer's Disease Neuroimaging Initiative
4 affiliations
  1. 1Department of Biomedical Engineering, Columbia University, New York, New York, USA.
  2. 2Neuroradiology Division, Department of Radiology, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Lenox Hill Hospital, New York, New York, USA.
  3. 3Department of Pathology, Nash Family Department of Neuroscience, Department of Artificial Intelligence & Human Health, Neuropathology Brain Bank & Research CoRE, Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York, USA.
  4. 4Department of Neurology, Columbia University Irving Medical Center, New York, New York, USA.
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Abstract

Introduction

Early neurofibrillary tau degeneration in the entorhinal cortex (EC) is a hallmark of Alzheimer's disease (AD) and aging. We propose a biomechanical cascade hypothesis, suggesting proximity to the tentorial incisura (TI) may render the EC susceptible to chronic mechanical stress, potentially contributing to tau pathology.Methods

We developed a neuroanatomical contact coefficient (NCC) to quantify EC-TI proximity using Alzheimer's Disease Neuroimaging Initiative multimodal imaging data (n = 47), stratifying participants into high and low adjacency groups.Results

Controlling for risk factors, EC tau positron emission tomography signal predicted conversion from mild cognitive impairment to AD only in the high-adjacency group (P = 0.036).Discussion

Findings identify EC-TI proximity as a potential, novel, anatomically grounded biomarker of AD risk. These findings are consistent with a previously unrecognized biomechanical contribution to EC tau vulnerability in sporadic AD and aging, opening new avenues for early detection, risk stratification, and mechanistically targeted prevention strategies.

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Cite

BibTeXRIS
BibTeX
@article{zhang2026structural,
  title = {{Structural compression and entorhinal vulnerability: Linking tentorial adjacency to tau burden and dementia progression.}},
  author = {Luyue Zhang and Ana M Franceschi and John F Crary and Frank A Provenzano and Alzheimer's Disease Neuroimaging Initiative},
  journal = {Alzheimer's \& dementia : the journal of the Alzheimer's Association},
  year = {2026},
  month = oct,
  doi = {10.1002/alz.71827},
  url = {https://europepmc.org/article/MED/42831470},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Structural compression and entorhinal vulnerability: Linking tentorial adjacency to tau burden and dementia progression.
AU  - Luyue Zhang
AU  - Ana M Franceschi
AU  - John F Crary
AU  - Frank A Provenzano
AU  - Alzheimer's Disease Neuroimaging Initiative
PY  - 2026
DA  - 2026/10/01
JO  - Alzheimer's & dementia : the journal of the Alzheimer's Association
DO  - 10.1002/alz.71827
UR  - https://europepmc.org/article/MED/42831470
AB  - Introduction  Early neurofibrillary tau degeneration in the entorhinal cortex (EC) is a hallmark of Alzheimer's disease (AD) and aging. We propose a biomechanical cascade hypothesis, suggesting proximity to the tentorial incisura (TI) may render the EC susceptible to chronic mechanical stress, potentially contributing to tau pathology.Methods  We developed a neuroanatomical contact coefficient (NCC) to quantify EC-TI proximity using Alzheimer's Disease Neuroimaging Initiative multimodal imaging data (n = 47), stratifying participants into high and low adjacency groups.Results  Controlling for risk factors, EC tau positron emission tomography signal predicted conversion from mild cognitive impairment to AD only in the high-adjacency group (P = 0.036).Discussion  Findings identify EC-TI proximity as a potential, novel, anatomically grounded biomarker of AD risk. These findings are consistent with a previously unrecognized biomechanical contribution to EC tau vulnerability in sporadic AD and aging, opening new avenues for early detection, risk stratification, and mechanistically targeted prevention strategies.
SN  - 1552-5260
SN  - 1552-5279
ER  -