Evidence map›Paper›PMID 21942371›Full record

ArticleAntioxidants & redox signaling2012

Influence of viral vector-mediated delivery of superoxide dismutase and catalase to the hippocampus on spatial learning and memory during aging.

Wei-Hua Lee, Ashok Kumar, Asha Rani, Jose Herrera, Jinze Xu, Shinichi Someya, Thomas C Foster

Abstract read
In one paragraph

Article in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Review
  3. Senescent neurophysiology: CaNeurobiology of learning and memory · 2019
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Re-Opening the Critical Window for Estrogen Therapy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  9. Article
  10. Impaired attention and synaptic senescence of the prefrontal cortex involves redox regulation of NMDA receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Linking redox regulation of NMDAR synaptic function to cognitive decline during aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  16. Article
  17. Article
  18. Role of estrogen receptor α and β in preserving hippocampal function during aging.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  19. Review
  20. A reversible early oxidized redox state that precedes macromolecular ROS damage in aging nontransgenic and 3xTg-AD mouse neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
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

7 authors at 1 institution in 1 country.

Wei-Hua LeeDepartment of Neuroscience, McKnight Brain Institute, University of Florida , Gainesville, Florida 32610-0244, USA.
Ashok Kumar
Asha Rani
Jose Herrera
Jinze Xu
Shinichi Someya
Thomas C Foster
University of Florida · US

Funding

University of Florida Older Americans Independence Center (OAIC)P30AG028740 · NIA · UNIVERSITY OF FLORIDA · PI Peihua Qiu · 2007 to 2026
$22.8M
UF Clinical and Translational Science AwardUL1TR000064 · NCATS · UNIVERSITY OF FLORIDA · PI NELSON, DAVID R · 2012 to 2014
$12.2M
Estrogen and cognition over the lifespanR01AG037984 · NIA · UNIVERSITY OF FLORIDA · PI FOSTER, THOMAS C, KUMAR, ASHOK · 2011 to 2022
$3.3M
Signaling cascades and memory deficits during agingR37AG036800 · NIA · UNIVERSITY OF FLORIDA · PI FOSTER, THOMAS C · 2010 to 2018
$2.6M
MECHANISMS FOR ALTERED SYNAPTIC FUNCTION DURING AGINGR01AG014979 · NIA · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI FOSTER, THOMAS C · 1998 to 2011
$2.5M
Cochlear Detoxification SystemR01DC014437 · NIDCD · UNIVERSITY OF FLORIDA · PI SOMEYA, SHINICHI · 2015 to 2019
$2.2M
Mitochondrial Thioredoxin, Caloric Restriction, and Age-related Hearing LossR01DC012552 · NIDCD · UNIVERSITY OF FLORIDA · PI SOMEYA, SHINICHI · 2013 to 2017
$1.9M
The Role of Glutathione Reductase in Age-related Hearing LossR03DC011840 · NIDCD · UNIVERSITY OF FLORIDA · PI SOMEYA, SHINICHI · 2011 to 2013
$432k
Estrogen and cognition over the lifespanR56AG037984 · NIA · UNIVERSITY OF FLORIDA · PI FOSTER, THOMAS C · 2010 to 2010
$271k
NCATS NIH HHS UL1 TR000064NIA NIH HHS AG014979NIA NIH HHS AG036800NIA NIH HHS AG037984NIA NIH HHS P30 AG028740NIA NIH HHS R01 AG014979NIA NIH HHS R37 AG036800NIA NIH HHS R56 AG037984NIDCD NIH HHS R01 DC012552NIDCD NIH HHS R01 DC014437NIDCD NIH HHS R03 DC011840
6 · The paper itself

Abstract

aimsStudies employing transgenic mice indicate that overexpression of superoxide dismutase 1 (SOD1) improves memory during aging. It is unclear whether the improvement is due to a lifetime of overexpression, decreasing the accumulation of oxidized molecules, or if increasing antioxidant enzymes in older animals could reduce oxidative damage and improve cognitive function. We used adeno-associated virus to deliver antioxidant enzymes (SOD1, SOD2, catalase [CAT], and SOD1+CAT) to the hippocampus of young (4 months) and aged (19 months) F344/BN F1 male rats and examined memory-related behavioral performance 1 month and 4 months postinjection.

resultsOverexpression of antioxidant enzymes reduced oxidative damage; however, memory function was not related to the level of oxidative damage. Increased expression of SOD1, initiated in advanced age, impaired learning. Increased expression of SOD1+CAT provided protection from impairments associated with overexpression of SOD1 alone and appears to guard against cognitive impairments in advanced age. INNOVATION: Viral vector gene delivery provides a novel approach to test the hypothesis that increased expression of antioxidant enzymes, specifically in hippocampal neurons, will provide protection from age-related cognitive decline. Further, expression of multiple vectors permits more detailed investigation of mechanistic pathways.

conclusionOxidative stress is a likely component of aging; however, it is unclear whether increased production of reactive oxygen species or the accumulation of oxidative damage is the primary cause of functional decline. The results provide support for the idea that altered redox-sensitive signaling rather than the accumulation of damage may be of greater significance in the emergence of age-related learning and memory deficits.

Indexed as

AgingAnimalsAntioxidantsCatalaseDependovirusGenetic VectorsHippocampusMaleMemoryMiceMice, TransgenicRatsRats, Inbred F344Spatial BehaviorSuperoxide DismutaseSuperoxide Dismutase-1AntioxidantsCatalaseSod1 protein, mouseSod1 protein, ratSuperoxide DismutaseSuperoxide Dismutase-1Superoxide Dismutase 2

Identifiers

PMID21942371
PMCPMC3246419
OpenAlexW2071749001

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.