Evidence map›Paper›PMID 37075128›Full record

ArticleScience translational medicine2023

Lateral mammillary body neurons in mouse brain are disproportionately vulnerable in Alzheimer's disease.

Wen-Chin Huang, Zhuyu Peng, Mitchell H Murdock, Liwang Liu, Hansruedi Mathys, Jose Davila-Velderrain, Xueqiao Jiang, Maggie Chen, Ayesha P Ng, TaeHyun Kim and 5 more

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Brain Nutrient Sensing: A Unifying Framework.Annual review of physiology · 2026
    Review
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  6. Article
  7. Article
  8. Article
  9. Cell-Type Specific Circuits in the Mammillary Body for Place and Object Recognition Memory.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  10. Article
  11. Article
  12. Article
  13. 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

15 authors at 3 institutions in 1 country.

Wen-Chin HuangPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-8419-6263
Zhuyu PengPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0003-1327-4337
Mitchell H MurdockPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-8625-624X
Liwang LiuPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0003-4689-1964
Hansruedi MathysPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0003-0186-2115
Jose Davila-VelderrainBroad Institute of MIT and Harvard, Cambridge, MA 02139, USA.ORCID 0000-0003-0271-6267
Xueqiao JiangPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-8073-1636
Maggie ChenDepartment of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-6573-4134
Ayesha P NgDepartment of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-8283-4436
TaeHyun KimPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0003-3871-5776
Fatema AbdurrobPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-5510-055X
Fan GaoPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0001-6832-3402
David A BennettRush Alzheimer's Disease Center, Rush University Medical Center, Chicago, IL 60612, USA.ORCID 0000-0003-3689-554X
Manolis KellisBroad Institute of MIT and Harvard, Cambridge, MA 02139, USA.ORCID 0000-0001-7113-9630
Li-Huei TsaiPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.ORCID 0000-0003-1262-0592
Massachusetts Institute of Technology · USBroad Institute · USRush University Medical Center · US

Funding

SUPPLEMENT TO RUSH ALZHEIMERS DISEASE CENTER COREP30AG010161 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI LEURGANS, SUE E. · 1991 to 2020
$49.1M
RISK FACTORS, PATHOLOGY, AND CLINICAL EXPRESSIONS OF ADR01AG015819 · NIA · RUSH UNIVERSITY MEDICAL CENTER · PI BENNETT, DAVID ALAN · 1998 to 2024
$21.4M
Epigenomic, transcriptional and cellular dissection of Alzheimer's variantsR01AG058002 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HYMAN, BRADLEY T., JAENISCH, RUDOLF · 2017 to 2021
$7.9M
Elucidating the Molecular Mechanisms of Neuropsychiatric Symptoms in Alzheimer's DiseaseR01AG062335 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KELLIS, MANOLIS, TSAI, LI-HUEI · 2018 to 2022
$6.5M
Single-cell transcriptional and epigenomic dissection of Alzheimer's Disease and Related DementiasU01NS110453 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KELLIS, MANOLIS, TSAI, LI-HUEI · 2018 to 2020
$4.0M
Demystifying Microglia in Aging and Alzheimer's DiseaseRF1AG054321 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI DE JAGER, PHILIP L, LEVIN, JOSHUA ZVI · 2016 to 2016
$4.0M
Cell type specific epigenetic analysis to understand complex mechanisms underlying Alzheimer's disease phenotypesRF1AG054012 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KELLIS, MANOLIS, TSAI, LI-HUEI · 2016 to 2016
$3.9M
Dissection of endosomal trafficking mechanisms in Alzheimer's DiseaseRF1AG062377 · NIA · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TSAI, LI-HUEI · 2018 to 2018
$3.6M
NIA NIH HHS P30 AG010161NIA NIH HHS R01 AG015819NIA NIH HHS R01 AG058002NIA NIH HHS R01 AG062335NIA NIH HHS RF1 AG054012NIA NIH HHS RF1 AG054321NIA NIH HHS RF1 AG062377NINDS NIH HHS U01 NS110453
6 · The paper itself

Abstract

The neural circuits governing the induction and progression of neurodegeneration and memory impairment in Alzheimer's disease (AD) are incompletely understood. The mammillary body (MB), a subcortical node of the medial limbic circuit, is one of the first brain regions to exhibit amyloid deposition in the 5xFAD mouse model of AD. Amyloid burden in the MB correlates with pathological diagnosis of AD in human postmortem brain tissue. Whether and how MB neuronal circuitry contributes to neurodegeneration and memory deficits in AD are unknown. Using 5xFAD mice and postmortem MB samples from individuals with varying degrees of AD pathology, we identified two neuronal cell types in the MB harboring distinct electrophysiological properties and long-range projections: lateral neurons and medial neurons. lateral MB neurons harbored aberrant hyperactivity and exhibited early neurodegeneration in 5xFAD mice compared with lateral MB neurons in wild-type littermates. Inducing hyperactivity in lateral MB neurons in wild-type mice impaired performance on memory tasks, whereas attenuating aberrant hyperactivity in lateral MB neurons ameliorated memory deficits in 5xFAD mice. Our findings suggest that neurodegeneration may be a result of genetically distinct, projection-specific cellular dysfunction and that dysregulated lateral MB neurons may be causally linked to memory deficits in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalHumansMammillary BodiesMemory DisordersMiceMice, TransgenicNeuronsAmyloid beta-Peptides

Identifiers

PMID37075128
PMCPMC10511020
OpenAlexW4366371460

What OpenQuestion holds

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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.