Evidence map›Paper›PMID 38192507›Full record

ReviewFrontiers in neuroscience2023

Understanding the molecular basis of resilience to Alzheimer's disease.

Kathleen S Montine, Eloïse Berson, Thanaphong Phongpreecha, Zhi Huang, Nima Aghaeepour, James Y Zou, Michael J MacCoss, Thomas J Montine

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
3.4field-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

8 citing papers in PubMed, 11 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Kathleen S MontineDepartment of Pathology, Stanford University, Stanford, CA, United States.
Eloïse BersonDepartment of Pathology, Stanford University, Stanford, CA, United States.
Thanaphong PhongpreechaDepartment of Pathology, Stanford University, Stanford, CA, United States.
Zhi HuangDepartment of Pathology, Stanford University, Stanford, CA, United States.
Nima AghaeepourDepartment of Anesthesiology, Stanford University, Stanford, CA, United States.
James Y ZouDepartment of Biomedical Data Science, Stanford University, Stanford, CA, United States.
Michael J MacCossDepartment of Genome Sciences, University of Washington, Seattle, WA, United States.
Thomas J MontineDepartment of Pathology, Stanford University, Stanford, CA, United States.
Stanford University · USUniversity of Washington · US

Funding

Project 4: Novel reagent development to enable molecular characterizationU19AG065156 · NIA · UNIVERSITY OF WASHINGTON · PI MACCOSS, MICHAEL · 2020 to 2024
$15.9M
Multi-omic functional assessment of novel AD variants using high-throughput and single-cell technologiesU01AG072573 · NIA · STANFORD UNIVERSITY · PI KUNDAJE, ANSHUL, MONTGOMERY, STEPHEN · 2021 to 2025
$8.3M
Molecular Phenotyping in Alzheimer's DiseaseRF1AG053959 · NIA · STANFORD UNIVERSITY · PI LARSON, ERIC B, MACCOSS, MICHAEL · 2016 to 2017
$4.1M
Machine Learning for Integrative Modeling of the Immune System in Clinical SettingsR35GM138353 · NIGMS · STANFORD UNIVERSITY · PI AGHAEEPOUR, NIMA · 2020 to 2024
$2.2M
Neuropathology of synapses in AD and ADRDRF1AG077443 · NIA · STANFORD UNIVERSITY · PI AGHAEEPOUR, NIMA, MONTINE, THOMAS J · 2023 to 2023
$2.2M
Neuropathology of synapses in AD and ADRDR01AG077443 · NIA · STANFORD UNIVERSITY · PI Nima Aghaeepour, Thomas J Montine · 2026 to 2026
$707k
NIA NIH HHS R01 AG077443NIA NIH HHS RF1 AG053959NIA NIH HHS RF1 AG077443NIA NIH HHS U01 AG072573NIA NIH HHS U19 AG065156NIGMS NIH HHS R35 GM138353
6 · The paper itself

Abstract

The cellular and molecular distinction between brain aging and neurodegenerative disease begins to blur in the oldest old. Approximately 15-25% of observations in humans do not fit predicted clinical manifestations, likely the result of suppressed damage despite usually adequate stressors and of resilience, the suppression of neurological dysfunction despite usually adequate degeneration. Factors during life may predict the clinico-pathologic state of resilience: cardiovascular health and mental health, more so than educational attainment, are predictive of a continuous measure of resilience to Alzheimer's disease (AD) and AD-related dementias (ADRDs). In resilience to AD alone (RAD), core features include synaptic and axonal processes, especially in the hippocampus. Future focus on larger and more diverse cohorts and additional regions offer emerging opportunities to understand this counterforce to neurodegeneration. The focus of this review is the molecular basis of resilience to AD.

Indexed as

agingcognitioncomputational modelsdementiamachine learningneuropathologic lesionproteomic analysis

Identifiers

PMID38192507
PMCPMC10773681
OpenAlexW4389978715

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.