Evidence map›Paper›PMID 34333070›Full record

ArticleBehavioural brain research2021

Reelin changes hippocampal learning in aging and Alzheimer's disease.

Austin T Marckx, Katja E Fritschle, Laurent Calvier, Joachim Herz

Open access · greenAbstract read
In one paragraph

Article in Behavioural brain research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Resveratrol Attenuates HMolecular neurobiology · 2025
    Article
  3. Review
  4. Genetic or therapeutic disruption of the Reelin/Apoer2 signaling pathway improves inflammatory arthritis outcomes.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
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  12. Article
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  15. 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

4 authors at 1 institution in 1 country.

Austin T MarckxDepartment of Molecular Genetics, UT Southwestern Medical Center, United States; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, United States. Electronic address: austin.marckx@utsouthwestern.edu.
Katja E FritschleDepartment of Molecular Genetics, UT Southwestern Medical Center, United States; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, United States.
Laurent CalvierDepartment of Molecular Genetics, UT Southwestern Medical Center, United States; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, United States.
Joachim HerzDepartment of Molecular Genetics, UT Southwestern Medical Center, United States; Center for Translational Neurodegeneration Research, UT Southwestern Medical Center, United States; Department of Neuroscience, UT Southwestern Medical Center, United States; Department of Neurology, UT Southwestern Medical Center, United States. Electronic address: joachim.herz@utsouthwestern.edu.
Southwestern Medical Center · US

Funding

Metabolism of the VLDL receptor and ApoE receptor 2R37HL063762 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2010 to 2019
$4.0M
Physiology and Pathophysiology of Apolipoprotein E receptor-2 splicing in Alzheimer's diseaseRF1AG053391 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.4M
Molecular Basis of Synaptic Suppression by ApoER01NS093382 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI HERZ, JOACHIM J · 2016 to 2020
$2.0M
NHLBI NIH HHS R37 HL063762NIA NIH HHS RF1 AG053391NINDS NIH HHS R01 NS093382
6 · The paper itself

Abstract

The hippocampal formation (HF) is a neuroanatomical region essential for learning and memory. As one of the earliest regions to display the histopathological hallmarks of Alzheimer's disease (AD), determining the specific mechanisms of the HF's vulnerability is of capital importance. Reelin, a glycoprotein crucial in cortical lamination during embryonic neurogenesis, has an uncommon expression pattern within the HF and has been implicated in both learning and AD pathogenesis. We hypothesized that Reelin deficiency would expedite behavioral impairments which accompany normal aging. Additionally, we hypothesized that Reelin deficiency in the presence of mutated human microtubule associated protein tau (MAPT) would further impair hippocampal function. To test our hypothesis, we utilized cohorts of aged mice, aged mice with Reelin conditional knockout (RcKO), and adult mice with both RcKO and MAPT in the Barnes maze and Trace fear conditioning. Consistent with prior literature, increased age in wild-type mice was sufficient to reduce spatial searching in the Barnes maze. Increased age both exacerbated spatial impairments and altered context learning in RcKO mice. Lastly, adult mice with both RcKO and the MAPT transgene displayed both the lowest age-of-onset and most severe spatial learning deficits. In conclusion, Reelin deficiency when combined with AD risk-factors produced consistent impairments in spatial memory tasks. Furthermore, our results further implicate Reelin's importance in both HF homeostasis and AD pathogenesis.

Indexed as

Alzheimer DiseaseCognitive DysfunctionHippocampusAge FactorsAgingAnimalsDisease Models, AnimalMaze LearningMiceMice, 129 StrainMice, KnockoutMice, TransgenicReelin Proteintau ProteinsMapt protein, mouseReelin ProteinReln protein, mousetau ProteinsAgingAlzheimer’s diseaseBarnes mazePS19ReelinTrace fear conditioning

Identifiers

PMID34333070
PMCPMC8483237
OpenAlexW3190320995

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.