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50/100

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Biomarkers

Topic: Brain proteins, microglia and lab models

Background and objectives Synaptic dysfunction and degeneration is a predominant feature of brain aging, and synaptic preservation buffers against Alzheimer disease (AD) protein-related brain atrophy. We tested whether CSF synaptic protein concentrations similarly moderate the effects of axonal injury, indexed by CSF neurofilament light [NfL]), on brain atrophy in clinically normal adults. Methods Clinically normal older adults enrolled in the observational Hillblom Aging Network study at the UCSF Memory and Aging Center completed baseline lumbar puncture and longitudinal brain MRI (mean scan [follow-up] = 2.6 [3.7 years]). CSF was assayed for synaptic proteins (synaptotagmin-1, synaptosomal-associated protein 25 [SNAP-25], neurogranin, growth-associated protein 43 [GAP-43]), axonal injury (NfL), and core AD biomarkers (ptau 181 /Aβ 42 ratio ; reflecting AD proteinopathy). Ten bilateral temporoparietal gray matter region of interest (ROIs) shown to be sensitive to clinical AD were summed to generate a composite temporoparietal ROI. Linear mixed-effects models tested statistical moderation of baseline synaptic proteins on baseline NfL-related temporoparietal trajectories, controlling for ptau 181 /Aβ 42 ratios. Results Forty-six clinically normal older adults (mean age = 70 years; 43% female) were included. Synaptic proteins exhibited small to medium correlations with NfL ( r range: 0.10-0.36). Higher baseline NfL, but not ptau 181 /Aβ 42 ratios, predicted steeper temporoparietal atrophy (NfL × time: β = -0.08, p 181 /Aβ 42 × time: β = -0.02, p = 0.31). SNAP-25, neurogranin, and GAP-43 significantly moderated NfL-related atrophy trajectories (-0.07 ≤ β's ≥ -0.06, p' s Discussion The association between baseline CSF NfL and longitudinal temporoparietal atrophy is accelerated by synaptic dysfunction and buffered by synaptic integrity. Beyond AD proteins, concurrent examination of in vivo axonal and synaptic biomarkers may improve detection of neural alterations that precede overt structural changes in AD-sensitive brain regions.

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APA 7th

Saloner, R., Fonseca, C., Paolillo, E. W., Asken, B. M., Djukic, N. A., Lee, S., et al. (2022). Combined Effects of Synaptic and Axonal Integrity on Longitudinal Gray Matter Atrophy in Cognitively Unimpaired Adults. Neurology. https://doi.org/10.1212/wnl.0000000000201165

Vancouver

Saloner R, Fonseca C, Paolillo EW, Asken BM, Djukic NA, Lee S, et al. Combined Effects of Synaptic and Axonal Integrity on Longitudinal Gray Matter Atrophy in Cognitively Unimpaired Adults. Neurology. 2022. doi:10.1212/wnl.0000000000201165. PMID: 36041868.

BibTeX

@article{saloner2022-36041868,
  author  = {Saloner, R. and Fonseca, C. and Paolillo, E. W. and Asken, B. M. and Djukic, N. A. and Lee, S. and Nilsson, J. and Brinkmalm, A. and others},
  title   = {{Combined Effects of Synaptic and Axonal Integrity on Longitudinal Gray Matter Atrophy in Cognitively Unimpaired Adults}},
  journal = {Neurology},
  year    = {2022},
  doi     = {10.1212/wnl.0000000000201165},
  pmid    = {36041868},
  url     = {https://doi.org/10.1212/wnl.0000000000201165}
}

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Key findings

Results Forty-six clinically normal older adults (mean age = 70 years; 43% female) were included.
SNAP-25, neurogranin, and GAP-43 significantly moderated NfL-related atrophy trajectories (-0.07 ≤ β's ≥ -0.06, p' s Discussion The association between baseline CSF NfL and longitudinal temporoparietal atrophy is accelerated by synaptic dysfunction and buffered by synaptic integrity.

Why it matters

In 46 clinically normal older adults, higher CSF synaptic proteins moderated the link between axonal injury marker NfL and later temporoparietal atrophy. This is a small longitudinal biomarker study and does not test any treatment, cure or prevention.

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Study details

Study designlongitudinal study
Evidence strengthModerate

How this study scored 50/100

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

Component	Points	Why
Journal tier	9 / 10	Tier 2 — leading specialty journal (Neurology)
Journal's citation record	4 / 4	Neurology: journal h-index 525 (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	3 / 5	2022 — within 6 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)
Randomised / blinded	0 / 2	No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	2 / 7	Cited 8 times (OpenAlex, 2026-10-10)
Citations per year	1 / 5	1.3 citations a year over 6 year(s) since 2022
Impact for its field and year	2 / 6	Cited 1.0× 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	1 / 4	Cited 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	2 / 4	Last-listed author Kaitlin Blackstone Casaletto: h-index 42 (OpenAlex, whole career)
Institution's track record	2 / 3	University College London: institution h-index 2,029 (OpenAlex)
Multi-centre collaboration	2 / 3	OpenAlex lists 7 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 36041868)
Free to read	0 / 2	Behind a paywall — scores zero
Total	50 / 100	—

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