Evidence map›Paper›PMID 39845935›Full record

ArticleFrontiers in neurology2024

Molecular profiling of frontal and occipital subcortical white matter hyperintensities in Alzheimer's disease.

Sulochan Malla, Annie G Bryant, Rojashree Jayakumar, Benjamin Woost, Nina Wolf, Andrew Li, Sudeshna Das, Susanne J van Veluw, Rachel E Bennett

Abstract read
In one paragraph

Article in Frontiers in neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Sulochan Malla *Department of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Annie G Bryant *Department of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Rojashree JayakumarDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Benjamin WoostDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Nina WolfDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Andrew LiDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Sudeshna DasDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Susanne J van VeluwDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.
Rachel E BennettDepartment of Neurology, Massachusetts General Hospital, Charlestown, MA, United States.

Funding

Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI STEVEN E ARNOLD · 2019 to 2026
$36.5M
Training and Dissemination CoreP41EB030006 · NIBIB · MASSACHUSETTS GENERAL HOSPITAL · PI Susie Yi Huang · 2020 to 2026
$10.9M
Microvascular Stress as a Pathway to Neurodegeneration in Alzheimer'sR01AG071567 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Rachel Elise Bennett · 2022 to 2026
$2.1M
NIA NIH HHS P30 AG062421NIA NIH HHS R01 AG071567NIBIB NIH HHS P41 EB030006
6 · The paper itself

Abstract

White matter hyperintensities (WMHs) are commonly detected on T2-weighted magnetic resonance imaging (MRI) scans, occurring in both typical aging and Alzheimer's disease (AD). Despite their frequent appearance and their association with cognitive decline in AD, the molecular factors contributing to WMHs remain unclear. In this study, we investigated the transcriptomic profiles of two commonly affected brain regions with coincident AD pathology-frontal subcortical white matter (frontal-WM) and occipital subcortical white matter (occipital-WM)-and compared with age-matched cognitively intact controls. Through RNA-sequencing in frontal- and occipital-WM bulk tissues, we identified an upregulation of genes associated with brain vasculature function in AD white matter. To further elucidate vasculature-specific transcriptomic features, we performed RNA-seq analysis on blood vessels isolated from these white matter regions, which revealed an upregulation of genes related to protein folding pathways. Finally, comparing gene expression profiles between AD individuals with high- versus low-WMH burden showed an increased expression of pathways associated with immune function. Taken together, our study characterizes the diverse molecular profiles of white matter changes in AD and provides mechanistic insights into the processes underlying AD-related WMHs.

Indexed as

Alzheimer’s diseaseangiogenesisblood vesselsbrain vasculatureheat shock proteins (HSPs)protein foldingwhite matter hyperintensities (WMHs)

Identifiers

PMID39845935
PMCPMC11753232

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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.