Evidence map›Paper›PMID 29406266›Full record

ArticleNeuroscience2018

Systemic or Forebrain Neuron-Specific Deficiency of Geranylgeranyltransferase-1 Impairs Synaptic Plasticity and Reduces Dendritic Spine Density.

David Hottman, Shaowu Cheng, Andrea Gram, Kyle LeBlanc, Li-Lian Yuan, Ling Li

Abstract read
In one paragraph

Article in Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-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, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. ACS chemical biology · 2022
    Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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
  12. 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.

David HottmanDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States.
Shaowu ChengDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States; College of Integrated Traditional Chinese and Western Medicine, Hunan University of Chinese Medicine, Yuelu District, Changsha, Hunan 410208, China.
Andrea GramDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States.
Kyle LeBlancDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States.
Li-Lian YuanDepartment of Neuroscience, University of Minnesota, Minneapolis, MN 55455, United States; Department of Physiology and Pharmacology, Des Moines University, Des Moines, IA 50312, United States.
Ling LiDepartment of Experimental and Clinical Pharmacology, University of Minnesota, Minneapolis, MN 55455, United States; Department of Pharmacology and Graduate Programs in Neuroscience, University of Minnesota, Minneapolis, MN 55455, United States. Electronic address: lil@umn.edu.
University of Minnesota · USDes Moines University · US

Funding

Training Grant: Functional Proteomics of AgingT32AG029796 · NIA · UNIVERSITY OF MINNESOTA · PI EDGAR A ARRIAGA, Douglas G Mashek · 2008 to 2026
$6.6M
Dysregulation of Protein Prenylation in the Pathogenesis of Alzheimer's DiseaseRF1AG056976 · NIA · UNIVERSITY OF MINNESOTA · PI DISTEFANO, MARK D, LI, LING · 2017 to 2017
$1.9M
Testing a Unique HDL Mimetic Peptide to Reverse ApoE4 Lipidation Deficiency and Alzheimer's NeuropathologyR21AG056025 · NIA · UNIVERSITY OF MINNESOTA · PI LI, LING · 2017 to 2018
$419k
NIA NIH HHS R21 AG056025NIA NIH HHS RF1 AG056976NIA NIH HHS T32 AG029796
6 · The paper itself

Abstract

Isoprenoids and prenylated proteins regulate a variety of cellular functions, including neurite growth and synaptic plasticity. Importantly, they are implicated in the pathogenesis of several diseases, including Alzheimer's disease (AD). Recently, we have shown that two protein prenyltransferases, farnesyltransferase (FT) and geranylgeranyltransferase-1 (GGT), have differential effects in a mouse model of AD. Haplodeficiency of either FT or GGT attenuates amyloid-β deposition and neuroinflammation but only reduction in FT rescues cognitive function. The current study aimed to elucidate the potential mechanisms that may account for the lack of cognitive benefit in GGT-haplodeficient mice, despite attenuated neuropathology. The results showed that the magnitude of long-term potentiation (LTP) was markedly suppressed in hippocampal slices from GGT-haplodeficient mice. Consistent with the synaptic dysfunction, there was a significant decrease in cortical spine density and cognitive function in GGT-haplodeficient mice. To further study the neuron-specific effects of GGT deficiency, we generated conditional forebrain neuron-specific GGT-knockout (GGT

Indexed as

Alkyl and Aryl TransferasesAnimalsBrainDendritic SpinesExcitatory Postsynaptic PotentialsFemaleGTP PhosphohydrolasesMaleMaze LearningMice, TransgenicNeuronal PlasticityPyramidal CellsSpatial MemoryTissue Culture TechniquesAlkyl and Aryl Transferasesgeranylgeranyltransferase type-IGTP Phosphohydrolasesdendritic spine densitygeranylgeranyltransferaseknockout mouse modelsprotein prenylationsmall GTPasessynaptic plasticity

Identifiers

PMID29406266
PMCPMC5816690
OpenAlexW2793712255

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.