Evidence map›Paper›PMID 22528861›Full record

ReviewNeuropsychology review2012

Translational rodent models of Korsakoff syndrome reveal the critical neuroanatomical substrates of memory dysfunction and recovery.

Lisa M Savage, Joseph M Hall, Leticia S Resende

Open access · greenAbstract readReview
In one paragraph

Review in Neuropsychology review, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Adolescent Alcohol and the Spectrum of Cognitive Dysfunction in Aging.Advances in experimental medicine and biology · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. The Inferior Colliculus in Alcoholism and Beyond.Frontiers in systems neuroscience · 2020
    Review
  10. Article
  11. Review
  12. Review
  13. The Regulatory Role of the Human Mediodorsal Thalamus.Trends in cognitive sciences · 2018
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Cognitive Decline and Recovery in Alcohol Abuse.Journal of molecular neuroscience : MN · 2016
    Review
  19. Article
  20. 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

3 authors at 2 institutions in 2 countries.

Lisa M SavageBehavioral Neuroscience Program, Department of Psychology, State University of New York at Binghamton, Binghamton, NY 13902, USA. lsavage@binghamton.edu
Joseph M Hall
Leticia S Resende
Binghamton University · USUniversidade Federal de Minas Gerais · BR

Funding

Cortical Biobehavioral Disruption after Thiamine Deficiency and Chronic AlcoholR01AA021775 · NIAAA · STATE UNIVERSITY OF NY,BINGHAMTON · PI SAVAGE, LISA M · 2014 to 2018
$2.3M
NIAAA NIH HHS R01 AA021775PHS HHS ARRA NINDS 054272-S1PHS HHS NINDS 054272
6 · The paper itself

Abstract

Investigation of the amnesic disorder Korsakoff Syndrome (KS) has been vital in elucidating the critical brain regions involved in learning and memory. Although the thalamus and mammillary bodies are the primary sites of neuropathology in KS, functional deactivation of the hippocampus and certain cortical regions also contributes to the chronic cognitive dysfunction reported in KS. The rodent pyrithiamine-induced thiamine deficiency (PTD) model has been used to study the extent of hippocampal and cortical neuroadaptations in KS. In the PTD model, the hippocampus, frontal and retrosplenial cortical regions display loss of cholinergic innervation, decreases in behaviorally stimulated acetylcholine release and reductions in neurotrophins. While PTD treatment results in significant impairment in measures of spatial learning and memory, other cognitive processes are left intact and may be recruited to improve cognitive outcome. In addition, behavioral recovery can be stimulated in the PTD model by increasing acetylcholine levels in the medial septum, hippocampus and frontal cortex, but not in the retrosplenial cortex. These data indicate that although the hippocampus and frontal cortex are involved in the pathogenesis of KS, these regions retain neuroplasticity and may be critical targets for improving cognitive outcome in KS.

Indexed as

Disease Models, AnimalAnimalsBrainCognition DisordersHumansKorsakoff SyndromeNeuroanatomyThiamine Deficiency

Identifiers

PMID22528861
PMCPMC5113815
OpenAlexW2072471833

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.