Evidence map›Paper›PMID 31259307›Full record

ReviewJournal of Alzheimer's disease reports2019

Medial Temporal Lobe Disconnection and Hyperexcitability Across Alzheimer's Disease Stages.

Lorenzo Pasquini, Farzaneh Rahmani, Somayeh Maleki-Balajoo, Renaud La Joie, Mojtaba Zarei, Christian Sorg, Alexander Drzezga, Masoud Tahmasian

Open access · diamondAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of Alzheimer's disease reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 83 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  9. Neuronal connectivity, behavioral, and transcriptional alterations associated with the loss of MARK2.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
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  17. Hippocampal metabolic subregions and networks: Behavioral, molecular, and pathological aging profiles.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
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  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 3 countries.

Lorenzo PasquiniDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
Farzaneh RahmaniSchool of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Somayeh Maleki-BalajooDepartment of Biomedical Engineering, Electrical Engineering Faculty, K.N. Toosi University of Technology, Tehran, Iran.
Renaud La JoieDepartment of Neurology, Memory and Aging Center, University of California, San Francisco, San Francisco, CA, USA.
Mojtaba ZareiInstitute of Medical Science and Technology, Shahid Beheshti University, Tehran, Iran.
Christian SorgDepartments of Neuroradiology, Klinikum rechts der Isar, Technische Universität München, Munich, Germany.
Alexander DrzezgaDepartment of Nuclear Medicine, University Hospital of Cologne, Cologne, Germany.
Masoud TahmasianInstitute of Medical Science and Technology, Shahid Beheshti University, Tehran, Iran.
Shahid Beheshti University · IRUniversity of California, San Francisco · USTehran University of Medical Sciences · IRTUM Klinikum · DEUniversity Hospital Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The posteromedial cortex (PMC) and medial temporal lobes (MTL) are two brain regions particularly vulnerable in Alzheimer's disease (AD). We have reviewed the spatiotemporal patterns of amyloid-β and tau accumulation, local MTL functional alterations and MTL-PMC network reconfiguration, and propose a model to relate these elements to each other. Functional and structural MTL-PMC disconnection happen concomitant with amyloid-β plaques and neurofibrillary tau accumulation within these same regions. Ongoing disconnection is accompanied by dysfunctional intrinsic local MTL circuit hyperexcitability, which exacerbates across distinct clinical stages of AD. Our overarching model proposes a sequence of events relating the spatiotemporal patterns of amyloid-β and tau accumulation to MTL-PMC disconnection and local MTL hyperexcitability. We hypothesize that cortical PMC amyloid-β pathology induces long-range information processing deficits through functional and structural MTL-PMC dysconnectivity at early disease stages, which in turn drives local MTL circuit hyperexcitability. Intrinsic local MTL circuit hyperexcitability subsequently accelerates local age-related tau deposition, facilitating tau spread from the MTL to the PMC, eventually resulting in extensive structural degeneration of white and grey matter as the disease advances. We hope that the present model may inform future longitudinal studies needed to test the proposed sequence of events.

Indexed as

Alzheimer’s diseaseamyloid-βdefault mode networkdisconnectionhyperexcitabilitymedial temporal lobemild cognitive impairmentposteromedial cortextau

Identifiers

PMID31259307
PMCPMC6597961
OpenAlexW2946291103

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.