Evidence map›Paper›PMID 24136196›Full record

ArticleThe Journal of biological chemistry2013

Farnesyltransferase haplodeficiency reduces neuropathology and rescues cognitive function in a mouse model of Alzheimer disease.

Shaowu Cheng, Dongfeng Cao, David A Hottman, LiLian Yuan, Martin O Bergo, Ling Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 15% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. ACS chemical biology · 2022
    Article
  8. Article
  9. A Farnesyltransferase Inhibitor Restores Cognitive Deficits inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Loss of TREM2 Confers Resilience to Synaptic and Cognitive Impairment in Aged Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  17. Article
  18. Review
  19. Article
  20. Review
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 2 institutions in 2 countries.

Shaowu ChengDepartments of Experimental and Clinical Pharmacology University of Minnesota, Minneapolis, MN, USA.
Dongfeng Cao
David A Hottman
LiLian Yuan
Martin O Bergo
Ling Li
University of Gothenburg · SEUniversity of Minnesota · US

Funding

Protective Mechanisms of Statins in Alzheimer's DiseaseR01AG031846 · NIA · UNIVERSITY OF MINNESOTA · PI LI, LING · 2008 to 2012
$1.5M
NIA NIH HHS AG031846NIA NIH HHS R01 AG031846
6 · The paper itself

Abstract

Isoprenoids and prenylated proteins have been implicated in the pathophysiology of Alzheimer disease (AD), including amyloid-β precursor protein metabolism, Tau phosphorylation, synaptic plasticity, and neuroinflammation. However, little is known about the relative importance of the two protein prenyltransferases, farnesyltransferase (FT) and geranylgeranyltransferase-1 (GGT), in the pathogenesis of AD. In this study, we defined the impact of deleting one copy of FT or GGT on the development of amyloid-β (Aβ)-associated neuropathology and learning/memory impairments in APPPS1 double transgenic mice, a well established model of AD. Heterozygous deletion of FT reduced Aβ deposition and neuroinflammation and rescued spatial learning and memory function in APPPS1 mice. Heterozygous deletion of GGT reduced the levels of Aβ and neuroinflammation but had no impact on learning and memory. These results document that farnesylation and geranylgeranylation play differential roles in AD pathogenesis and suggest that specific inhibition of protein farnesylation could be a potential strategy for effectively treating AD.

Indexed as

CognitionGene DeletionAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalFarnesyltranstransferaseMemoryMiceMice, TransgenicProteolysisAmyloid beta-PeptidesFarnesyltranstransferaseAlzheimers DiseaseAmyloidIsoprenoidLearning and MemoryNeuroinflammationProtein PrenylationTransgenic Mice

Identifiers

PMID24136196
PMCPMC3861644
OpenAlexW1971235233

What OpenQuestion holds

Textmetadata
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.