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44/100

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Brain scans and imaging

Topic: Amyloid, tau and blood-test diagnosis

Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown. Baseline TSPO, amyloid, and tau PET as well as T1 MRI from the longitudinal imaging of microglial activation in different clinical variants of Alzheimer disease study were adjusted for age, sex, body mass index, APOE4 status, TSPO genotype, and intracranial total volume. Imaging outcomes were standardized against controls, visualized across the brain, and placed along a pseudo-longitudinal timeline using disease duration. Microglia density follows the spatial distribution of tau in amyloid-positive individuals and that of neurodegeneration in amyloid-negative individuals. The magnitude, location, and timing of elevated microglia density relative to amyloid, tau, and neurodegeneration is specific to different clinical subtypes of Alzheimer disease.

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

APA 7th

Houlihan, H. M., Guzman, D., Smith, A. P., Sanchez, T. A., Johnson, A. S., Kreisl, W. C., et al. (2025). Neuroimaging Compendium of Microglia, Amyloid, Tau, and Neurodegeneration Across Clinical Variants of Alzheimer Disease. Alzheimer Disease & Associated Disorders. https://doi.org/10.1097/wad.0000000000000707

Vancouver

Houlihan HM, Guzman D, Smith AP, Sanchez TA, Johnson AS, Kreisl WC, et al. Neuroimaging Compendium of Microglia, Amyloid, Tau, and Neurodegeneration Across Clinical Variants of Alzheimer Disease. Alzheimer Disease & Associated Disorders. 2025. doi:10.1097/wad.0000000000000707. PMID: 41288284.

BibTeX

@article{houlihan2025-41288284,
  author  = {Houlihan, Hannah M. and Guzman, Diana and Smith, Anna P. and Sanchez, Tiago Arruda and Johnson, Aubrey S. and Kreisl, William Charles and Cosentino, Stephanie and Noble, James McC. and others},
  title   = {{Neuroimaging Compendium of Microglia, Amyloid, Tau, and Neurodegeneration Across Clinical Variants of Alzheimer Disease}},
  journal = {Alzheimer Disease \& Associated Disorders},
  year    = {2025},
  doi     = {10.1097/wad.0000000000000707},
  pmid    = {41288284},
  url     = {https://doi.org/10.1097/wad.0000000000000707}
}

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Key findings

Alzheimer disease and its clinical variants have characteristic spatial and temporal progression patterns of amyloid and tau driving symptomatology, but the distribution of microglia density, as measured by 18kDa translocator protein (TSPO) PET, is unknown.
Baseline TSPO, amyloid, and tau PET as well as T1 MRI from the longitudinal imaging of microglial activation in different clinical variants of Alzheimer disease study were adjusted for age, sex, body mass index, APOE4 status, TSPO genotype, and intracranial total volume.
Imaging outcomes were standardized against controls, visualized across the brain, and placed along a pseudo-longitudinal timeline using disease duration.
Microglia density follows the spatial distribution of tau in amyloid-positive individuals and that of neurodegeneration in amyloid-negative individuals.
The magnitude, location, and timing of elevated microglia density relative to amyloid, tau, and neurodegeneration is specific to different clinical subtypes of Alzheimer disease.

Why it matters

This study found that microglia density, measured by TSPO PET, follows the spatial distribution of tau in amyloid-positive individuals and of neurodegeneration in amyloid-negative individuals. The magnitude, location, and timing of elevated microglia density differed across clinical subtypes of Alzheimer's disease.

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Study details

Study designlongitudinal study
Evidence strengthModerate

How this study scored 44/100

Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for sample size, effect reported, studied in people and randomized / blinded because the record does not state it.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Alzheimer Disease & Associated Disorders)
Journal's citation record	1 / 4	Alzheimer Disease & Associated Disorders: journal h-index 131 (OpenAlex, 2026-10-29)
Study design	7 / 12	A longitudinal study following the same people over 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	0 / 4	Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported	0 / 3	No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people	0 / 3	Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	1 / 7	Cited 2 times (OpenAlex, 2026-10-10)
Citations per year	0 / 5	0.7 citations a year over 3 year(s) since 2025
Impact for its field and year	2 / 6	Cited 1.1× 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 2 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Patrick J. Lao: h-index 28 (OpenAlex, whole career)
Institution's track record	2 / 3	Columbia University: institution h-index 1,824 (OpenAlex)
Multicenter collaboration	1 / 3	OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 41288284)
Free to read	2 / 2	Free to read
Total	44 / 100	—

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