Evidence map›Paper›PMID 27567878›Full record

ReviewJournal of Alzheimer's disease : JAD2017

Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons.

Ravi Rajmohan, P Hemachandra Reddy

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07667478 (NON-INVASIVE BRAIN STIMULATION FOR MEMORY LOSS IN EARLY ALZHEIMER'S DISEASE), which is not on this map. Cited by 342 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
342citing papers in PubMed, 6 pooled it
6.6field-weighted citation impact, top 3% 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.

NCT07667478 narecruitingnot on this mapstarted 2026, after this paper: background citation

Non-invasive brain stimulation for memory loss in early alzheimer's disease

TypeinterventionalSponsorChi-Ying (Roy) LinRan2026 to 2031Enrolled40ConditionsAlzheimer s Disease, Mild Cognitive Impairment (MCI) Due to Alzheimer's Disease, Mild DementiaArmsrepetitive transcranial magnetic stimulation (rTMS), sham repetitive transcranial magnetic stimulation rTMS
3 · Its place in the literature

Who cites it

342 citing papers in PubMed, 6 syntheses or guidelines pooled it, 655 citations in OpenAlex.

  1. Pooled it
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  4. Oral Health as a Risk Factor for Alzheimer Disease.The journal of prevention of Alzheimer's disease · 2024
    Pooled it
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  7. Trial
  8. Article
  9. Fraxetin Ameliorates Cognitive Impairment in STZ-Induced Mice: Involvement of Suppressed Microglial Hyperactivation and Improved Mitochondrial Dysfunction.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026
    Article
  10. Unveiling the pathogenesis and therapeutic strategies of Alzheimer's disease through cuproptosis.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
    Review
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282 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Ravi RajmohanDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
P Hemachandra ReddyDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Texas Tech University · US

Funding

Dynamin-Related Protein 1 and Mitochondrial Fragmentation in Alzheimer's DiseaseR01AG042178 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2012 to 2016
$2.0M
Voltage-Dependent Anion Channel and Neurodegeneration in Alzheimer's DiseaseR01AG047812 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2014 to 2018
$1.9M
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812
6 · The paper itself

Abstract

Amyloid-beta (Aβ) and hyperphosphorylated tau are hallmark lesions of Alzheimer's disease (AD). However, the loss of synapses and dysfunctions of neurotransmission are more directly tied to disease severity. The role of these lesions in the pathoetiological progression of the disease remains contested. Biochemical, cellular, molecular, and pathological studies provided several lines of evidence and improved our understanding of how Aβ and hyperphosphorylated tau accumulation may directly harm synapses and alter neurotransmission. In vitro evidence suggests that Aβ and hyperphosphorylated tau have both direct and indirect cytotoxic effects that affect neurotransmission, axonal transport, signaling cascades, organelle function, and immune response in ways that lead to synaptic loss and dysfunctions in neurotransmitter release. Observations in preclinical models and autopsy studies support these findings, suggesting that while the pathoetiology of positive lesions remains elusive, their removal may reduce disease severity and progression. The purpose of this article is to highlight the need for further investigation of the role of tau in disease progression and its interactions with Aβ and neurotransmitters alike.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsHumansPhosphorylationSynapsestau ProteinsAmyloid beta-Peptidestau ProteinsAmyloidneurotransmitterssynapsetau

Identifiers

PMID27567878
PMCPMC5793225
OpenAlexW2510053021

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

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.