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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Vascular contributions

Topic: Brain proteins, microglia and lab models

White matter hyperintensities (WMH) are associated with cortical thinning in distant brain regions. However, it is currently unclear how WMH affect neurodegeneration in early Alzheimer's disease (AD). Here, we investigated associations between WMH and cortical thickness in temporal regions involved in early AD (AD cortical signature), while correcting for regional amyloid and tau accumulation assessed by PET. We performed cross-sectional (n = 551), and longitudinal (n = 125) analyses in older adults without dementia, also stratified by amyloid positivity. We evaluated WMH volume - as a measure of the global burden of WMH-related cerebrovascular pathology (GB-WMH) - and investigated the role of deep versus periventricular WMH. We also tested whether a higher focal burden of WMH in specific tracts connected to AD signature regions (FB-WMH) would lead to greater cortical thinning than expected solely from GB-WMH. We performed exploratory analyses in other brain regions to check the specificity of our findings to the temporal AD signature. GB-WMH damage, especially involving periventricular WMH, was cross-sectionally (not longitudinally) associated with cortical thinning in the fusiform, inferior and middle temporal gyri. Stronger associations were found in amyloid-positive individuals, including for the entorhinal cortex. Effects were mostly confined to regions of the temporal AD signature. FB-WMH did not yield higher cortical thinning than expected solely by GB-WMH. Cerebrovascular disease is associated with cortical thinning of temporal regions involved in early AD. Interventions aimed at improving cerebrovascular health might help to mitigate neurodegeneration in these regions.

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

APA 7th

Leone, R., & Kobeleva, X. (2025). White matter hyperintensities contribute to early cortical thinning in addition to tau in aging. Neurobiology of Aging. https://doi.org/10.1016/j.neurobiolaging.2025.07.007

Vancouver

Leone R, Kobeleva X. White matter hyperintensities contribute to early cortical thinning in addition to tau in aging. Neurobiology of Aging. 2025. doi:10.1016/j.neurobiolaging.2025.07.007. PMID: 40712373.

BibTeX

@article{leone2025-40712373,
  author  = {Leone, Riccardo and Kobeleva, Xenia},
  title   = {{White matter hyperintensities contribute to early cortical thinning in addition to tau in aging}},
  journal = {Neurobiology of Aging},
  year    = {2025},
  doi     = {10.1016/j.neurobiolaging.2025.07.007},
  pmid    = {40712373},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2025.07.007}
}

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Key findings

White matter hyperintensities (WMH) are associated with cortical thinning in distant brain regions.
We evaluated WMH volume - as a measure of the global burden of WMH-related cerebrovascular pathology (GB-WMH) - and investigated the role of deep versus periventricular WMH.
We performed exploratory analyses in other brain regions to check the specificity of our findings to the temporal AD signature.
GB-WMH damage, especially involving periventricular WMH, was cross-sectionally (not longitudinally) associated with cortical thinning in the fusiform, inferior and middle temporal gyri.
Cerebrovascular disease is associated with cortical thinning of temporal regions involved in early AD.

Why it matters

In this study of older adults without dementia, global white matter hyperintensity burden, especially periventricular, was cross-sectionally associated with cortical thinning in temporal regions involved in early Alzheimer's disease, with stronger associations in amyloid-positive individuals. The associations were not found longitudinally, and the study does not test any treatment, cure, or prevention.

Study details

Study designcross-sectional
Participants551
Evidence strengthModerate

How this study scored 45/100

Published in a peer-reviewed journal, and it is a snapshot of people at one point in time. Scored zero for effect reported and randomised / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Neurobiology of Aging)
Journal's citation record	3 / 4	Neurobiology of Aging: journal h-index 263 (OpenAlex, 2026-10-29)
Study design	4 / 12	A snapshot of people at one point in time
Strength of evidence	3 / 5	Rated “moderate” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	4 / 5	2025 — within 3 year(s) of the newest study here
Sample size	2 / 4	551 participants
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	3 / 3	Studied in people (participant count stated)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	1 / 7	Cited 1 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.3 citations a year over 3 year(s) since 2025
Impact for its field and year	1 / 6	Cited 0.6× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	0 / 6	No other study in this library cites it
Still being cited	0 / 4	Cited 1 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	1 / 4	Last-listed author Xenia Kobeleva: h-index 19 (OpenAlex, whole career)
Institution's track record	1 / 3	University of Bonn: institution h-index 1,072 (OpenAlex)
Multi-centre collaboration	1 / 3	OpenAlex lists 3 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 40712373)
Free to read	2 / 2	Free to read
Total	45 / 100	—

What each of these 20 components measures, and what this score is not →

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