Evidence map›Paper›PMID 22466291›Full record

ArticleBrain : a journal of neurology2012

False recognition in a mouse model of Alzheimer's disease: rescue with sensory restriction and memantine.

Carola Romberg, Stephanie M McTighe, Christopher J Heath, Daniel J Whitcomb, Kwangwook Cho, Timothy J Bussey, Lisa M Saksida

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 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
3.1field-weighted citation impact, top 8% 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, 52 citations in OpenAlex.

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  7. Differential vulnerability of hippocampal CA3-CA1 synapses to Aβ.Acta neuropathologica communications · 2022
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  8. A Neuroscience Primer for Integrating Geroscience With the Neurobiology of Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022
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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

7 authors at 3 institutions in 1 country.

Carola RombergDepartment of Experimental Psychology, University of Cambridge, Cambridge CB2 3EB, UK. carola.romberg@gmail.com
Stephanie M McTighe
Christopher J Heath
Daniel J Whitcomb
Kwangwook Cho
Timothy J Bussey
Lisa M Saksida
Wellcome Trust · GBUniversity of Bristol · GBUniversity of Cambridge · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G003963/1Medical Research Council G0001354Medical Research Council MC_G1000734Wellcome Trust 089703Wellcome Trust 093875
6 · The paper itself

Abstract

Alzheimer's disease is commonly regarded as a loss of memory for past events. However, patients with Alzheimer's disease seem not only to forget events but also to express false confidence in remembering events that have never happened. How and why false recognition occurs in such patients is currently unknown, and treatments targeting this specific mnemonic abnormality have not been attempted. Here, we used a modified object recognition paradigm to show that the tgCRND8 mouse-which overexpresses amyloid β and develops amyloid plaques similar to those in the brains of patients with Alzheimer's disease-exhibits false recognition. Furthermore, we found that false recognition did not occur when tgCRND8 mice were kept in a dark, quiet chamber during the delay, paralleling previous findings in patients with mild cognitive impairment, which is often considered to be prodromal Alzheimer's disease. Additionally, false recognition did not occur when mice were treated with the partial N-methyl-d-aspartic acid receptor antagonist memantine. In a subsequent experiment, we found abnormally enhanced N-methyl-d-aspartic acid receptor-dependent long-term depression in these mice, which could be normalized by treatment with memantine. We suggest that Alzheimer's disease typical amyloid β pathology leads to aberrant synaptic plasticity, thereby making memory representations more susceptible to interfering sensory input, thus increasing the likelihood of false recognition. Parallels between these findings and those from the literature on Alzheimer's disease and mild cognitive impairment suggest a mechanism underlying false recognition in these patients. The false recognition phenomenon may provide a novel paradigm for the discovery of potential therapies to treat the mnemonic dysfunction characteristic of this disease.

Indexed as

Alzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalElectric StimulationLong-Term Synaptic DepressionMemantineMiceMice, TransgenicPlaque, AmyloidRecognition, PsychologySensory DeprivationTemporal LobeAmyloid beta-Protein PrecursorMemantine

Identifiers

PMID22466291
PMCPMC3381719
OpenAlexW2051514662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.