Evidence map›Paper›PMID 33157321›Full record

ReviewAgeing research reviews2021

Synaptic basis of Alzheimer's disease: Focus on synaptic amyloid beta, P-tau and mitochondria.

Albin John, P Hemachandra Reddy

Open access · greenAbstract readReview
In one paragraph

Review in Ageing research reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 197 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
197citing papers in PubMed, 5 pooled it
20.8field-weighted citation impact, top 1% 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

197 citing papers in PubMed, 5 syntheses or guidelines pooled it, 344 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Article
  7. The Alzheimer's disease risk gene SORL1 is a regulator of excitatory neuronal function.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

137 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.

Albin JohnDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA.
P Hemachandra ReddyDepartment of Internal Medicine, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Neurology, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Public Health, Graduate School of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA; Department of Speech, Language, and Hearing Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA. Electronic address: Hemachandra.reddy@ttuhsc.edu.
Texas Tech University · US

Funding

Mitochondrial Molecules in Alzheimer's Disease and Other TauopathiesR01AG069333 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2020 to 2023
$3.4M
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
Mitochondrial Fragmentation and Neurodegeneration in Huntington's DiseaseR01NS105473 · NINDS · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2017 to 2021
$1.8M
Small Molecules as Therapeutic Targets for Alzheimer's DiseaseR56AG060767 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2019 to 2019
$699k
MicroRNA-455-3p and Alzheimer's DiseaseR56AG066347 · NIA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI REDDY, P. HEMACHANDRA · 2020 to 2020
$586k
NIA NIH HHS R01 AG042178NIA NIH HHS R01 AG047812NIA NIH HHS R01 AG069333NIA NIH HHS R56 AG060767NIA NIH HHS R56 AG066347NINDS NIH HHS R01 NS105473
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive and synaptic failure disease. Despite the many years of research, AD still harbors many secrets. As more of the world's population grows older, researchers are striving to find greater information on disease progression and pathogenesis. Identifying and treating the markers of this disease, or better yet, preventing it all together, are the hopes of those investing in this field of study. Several years of research revealed that synaptic pathology and mitochondrial oxidative damage are early events in disease progression. Loss of synapses and synaptic damage are the best correlates of cognitive deficits found in AD patients. As the disease progresses, there are significant changes at the synapse. These changes can both shed greater light onto the progression of the disease and serve as markers and therapeutic targets. This article addresses the mechanisms of synaptic action, mitochondrial regulation/dysregulation, resulting synaptic changes caused by amyloid beta and phosphorylated tau in AD progression. This article also highlights recent developments of risk factors, genetics and ApoE4 involvement, factors related to synaptic damage and loss, mislocalization of amyloid beta and phosphorylated tau, mitophagy, microglial activation and synapse-based therapies in AD. Furthermore, impairments in LTD and reactivation of microglia are discussed.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4HumansMitochondriaReelin ProteinSynapsestau ProteinsAmyloid beta-PeptidesApolipoprotein E4Reelin ProteinRELN protein, humantau ProteinsAlzheimer’s diseaseAmyloid betaAmyloid precursor proteinApoE4FYNMicrogliaMitochondriaMitochondrial dynamicsMitophagyReelinSynapseTau

Identifiers

PMID33157321
PMCPMC7770124
OpenAlexW3097560931

What OpenQuestion holds

Textmetadata
LicenceTDM
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.