Evidence map›Paper›PMID 32804096›Full record

ReviewJournal of Alzheimer's disease : JAD2020

Collapsin Response Mediator Proteins: Novel Targets for Alzheimer's Disease.

Tam T Quach, Aubin Moutal, Rajesh Khanna, Nicholas P Deems, Anne-Marie Duchemin, Ruth M Barrientos

Open access · greenAbstract readReview
In one paragraph

Review in Journal of Alzheimer's disease : JAD, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
0.9field-weighted citation impact, top 30% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Article
  5. Article
  6. NMDARs in Alzheimer's Disease: Between Synaptic and Extrasynaptic Membranes.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Article
  9. Review
  10. Review
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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

6 authors at 3 institutions in 1 country.

Tam T QuachInstitute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Aubin MoutalDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA.
Rajesh KhannaDepartment of Pharmacology, University of Arizona, Tucson, AZ, USA.
Nicholas P DeemsInstitute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Anne-Marie DucheminDepartment of Psychiatry and Behavioral Health, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Ruth M BarrientosInstitute for Behavioral Medicine Research, Wexner Medical Center, The Ohio State University, Columbus, OH, USA.
Institute for Behavioral Medicine · USUniversity of Arizona · USThe Ohio State University Wexner Medical Center · US

Funding

Neuroinflammation, Inflammatory Challenge, and MemoryR01AG028271 · NIA · UNIVERSITY OF COLORADO · PI MAIER, STEVEN F · 2006 to 2016
$3.8M
CRMP2, mitochondria, and Huntington’s diseaseR01NS098772 · NINDS · INDIANA UNIVERSITY INDIANAPOLIS · PI BRUSTOVETSKY, NICKOLAY, KHANNA, RAJESH · 2017 to 2021
$2.8M
Neuroinflammation, Inflammatory Challenge, and MemoryRF1AG028271 · NIA · UNIVERSITY OF COLORADO · PI BARRIENTOS, RUTH M, MAIER, STEVEN F · 2018 to 2021
$2.4M
Restorative gene therapy on hippocampal spino-dendritic abnormalities: a focus on Alzheimer’s diseaseR21AG071133 · NIA · OHIO STATE UNIVERSITY · PI BARRIENTOS, RUTH M · 2021 to 2022
$435k
Exploring HFD-induced alterations in long-term potentiation in aged hippocampus and amygdalaR03AG067061 · NIA · OHIO STATE UNIVERSITY · PI BARRIENTOS, RUTH M · 2020 to 2021
$156k
NIA NIH HHS R01 AG028271NIA NIH HHS R03 AG067061NIA NIH HHS R21 AG071133NIA NIH HHS RF1 AG028271NINDS NIH HHS R01 NS098772
6 · The paper itself

Abstract

Numerous experimental and postmortem studies have increasingly reported dystrophic axons and dendrites, and alterations of dendritic spine morphology and density in the hippocampus as prominent changes in the early stages of Alzheimer's disease (AD). Furthermore, these alterations tend to correlate well with the progressive cognitive decline observed in AD. For these reasons, and because these neurite structures have a capacity to re-grow, re-establish lost connections, and are critical for learning and memory, there is compelling evidence to suggest that therapeutic interventions aimed at preventing their degradation or promoting their regrowth may hold tremendous promise in preventing the progression of AD. In this regard, collapsin response mediator proteins (CRMPs), a family of phosphoproteins playing a major role in axon guidance and dendritic growth, are especially interesting. The roles these proteins play in neurons and immune cells are reviewed here.

Indexed as

Alzheimer DiseaseAnimalsAxonsCollapsin Response Mediator Protein 1DendritesDrug Delivery SystemsHippocampusHumansImmunologic FactorsNerve Tissue ProteinsNeuritesNeuronsProtein IsoformsCollapsin Response Mediator Protein 1CRMP1 protein, humanImmunologic FactorsNerve Tissue ProteinsProtein IsoformsAxon guidancedendrite regenerationhippocampusmemory

Identifiers

PMID32804096
PMCPMC7579750
OpenAlexW3048651332

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.