Evidence map›Paper›PMID 40468412›Full record

ArticleMolecular neurodegeneration2025

The UNC5C T835M mutation associated with Alzheimer's disease leads to neurodegeneration involving oxidative stress and hippocampal atrophy in aged mice.

Devi Krishna Priya Karunakaran, Makenna Ley, Joanna Guo, Ammaarah Khatri, Katherine Sadleir, Jelena Popovic, Arun Kumar Upadhyay, Jeffrey Savas, Daniele Procissi, Jasvinder Atwal and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular neurodegeneration, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Devi Krishna Priya KarunakaranDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Makenna LeyDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Joanna GuoDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Ammaarah KhatriDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Katherine SadleirDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Jelena PopovicDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Arun Kumar UpadhyayDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Jeffrey SavasDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Daniele ProcissiCenter for Preclinical Imaging Core Facility, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA.
Jasvinder AtwalDepartment of Neuroscience, South San Francisco, Genentech, CA, USA.
Robert VassarDepartment of Neurology, Feinberg School of Medicine, Northwestern University, Chicago, IL, 60611, USA. r-vassar@northwestern.edu.ORCID 0000-0002-1358-504X

Funding

Understanding Amyloid Pathology - Multiomic Activity Imaging of Plaque Formation Dynamics (AmyMAP)R01AG078796 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Jeffrey Nicholas Savas · 2022 to 2026
$2.7M
Orbitrap Eclipse Mass Spectrometer for Northwestern University Neuroproteomic Collaboration HubS10OD032464 · OD · NORTHWESTERN UNIVERSITY · PI SAVAS, JEFFREY NICHOLAS · 2023 to 2023
$1.3M
Alzheimer's Association AARF-16-443173NIA NIH HHS AG0577277NIA NIH HHS R01 AG078796NIH HHS S10 OD032464
6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by amyloid plaques, neurofibrillary tangles, and synaptic and neuronal loss. Recently, a rare autosomal dominant coding mutation, T835M, in the Un-coordinated 5c (UNC5C) netrin receptor gene was segregated with late-onset AD (LOAD). Overexpression of T835M in primary hippocampal neurons increased cell death in response to neurotoxic stimuli including beta-amyloid (Aβ) suggesting a mechanism by which T835M may confer increased risk of LOAD. However, the molecular mechanism of T835M-mediated cell death remained under explored. Toward this end, we generated a mouse T835M knock-in (Unc5c

Indexed as

Alzheimer DiseaseHippocampusNerve DegenerationNetrin ReceptorsOxidative StressAgingAnimalsAtrophyDisease Models, AnimalMiceMice, TransgenicMutationNeuronsNetrin Receptors

Identifiers

PMID40468412
PMCPMC12135551

What Socratic 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 Socratic graph.