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55/100

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Biomarkers

Topic: Amyloid, tau and blood-test diagnosis

Objective To test the hypothesis that cognitively unimpaired individuals with Alzheimer disease (AD) neuropathology differ from individuals with AD dementia on biomarkers of neurodegeneration, synaptic dysfunction, and glial activation. Methods In a cross-sectional study, adult participants >70 years old (n = 79, age 77.1 ± 5.3 years) underwent comprehensive cognitive evaluation and CSF collection, which was assayed for markers of amyloid, phosphorylated tau (p-tau), neurodegeneration (neurofilament light protein [NFL] and total tau), synaptic dysfunction (neurogranin), and glial activation (chitinase-3-like protein 1 [YKL-40]). Participants were divided into 3 groups based on diagnosis and p-tau/β-amyloid 42 (Aβ 42 ): those with low p-tau/Aβ 42 and unimpaired cognition were classified as controls (n = 25); those with high p-tau/Aβ 42 diagnosed with AD-dementia or AD-mild cognitive impairment were classified as AD-Dementia (n = 40); and those with high p-tau/Aβ 42 but unimpaired cognition were classified as mismatches (n = 14). A similar, secondary analysis was performed with no age exclusion criteria (n = 411). Results In both the primary and secondary analyses, biomarker levels between groups were compared with the use of analysis of covariance while controlling for age and demographic variables. Despite p-tau/Aβ 42 and Aβ 42 /Aβ 40 levels comparable to those of the AD-Dementia group, mismatches had significantly lower levels of NFL and total tau. While not significantly lower than the AD-Dementia group on YKL-40 and neurogranin, mismatches were also not significantly different from controls. Conclusions These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. This finding provides insight into the biological processes phenotypic of dementia and supports monitoring multiple biomarkers in individuals positive for AD neuropathology.

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APA 7th

Merluzzi, A. P., Carlsson, C. M., Johnson, S. C., Schindler, S. E., Asthana, S., Blennow, K., et al. (2018). Neurodegeneration, synaptic dysfunction, and gliosis are phenotypic of Alzheimer dementia. Neurology. https://doi.org/10.1212/wnl.0000000000005901

Vancouver

Merluzzi AP, Carlsson CM, Johnson SC, Schindler SE, Asthana S, Blennow K, et al. Neurodegeneration, synaptic dysfunction, and gliosis are phenotypic of Alzheimer dementia. Neurology. 2018. doi:10.1212/wnl.0000000000005901. PMID: 29959263.

BibTeX

@article{merluzzi2018-29959263,
  author  = {Merluzzi, A. P. and Carlsson, C. M. and Johnson, S. C. and Schindler, S. E. and Asthana, S. and Blennow, K. and Zetterberg, H. and Bendlin, B. B.},
  title   = {{Neurodegeneration, synaptic dysfunction, and gliosis are phenotypic of Alzheimer dementia}},
  journal = {Neurology},
  year    = {2018},
  doi     = {10.1212/wnl.0000000000005901},
  pmid    = {29959263},
  url     = {https://doi.org/10.1212/wnl.0000000000005901}
}

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Key findings

Results In both the primary and secondary analyses, biomarker levels between groups were compared with the use of analysis of covariance while controlling for age and demographic variables.
Despite p-tau/Aβ 42 and Aβ 42 /Aβ 40 levels comparable to those of the AD-Dementia group, mismatches had significantly lower levels of NFL and total tau.
While not significantly lower than the AD-Dementia group on YKL-40 and neurogranin, mismatches were also not significantly different from controls.
Conclusions These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired.

Why it matters

Among 79 older adults, those with Alzheimer's disease pathology but unimpaired cognition had lower levels of neurofilament light and total tau than those with Alzheimer's dementia, while levels of YKL-40 and neurogranin were not significantly different from controls. This suggests that neurodegeneration and synaptic dysfunction markers, rather than amyloid or tau alone, distinguish people with dementia from those with pathology but preserved cognition.

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Study details

Study designcross-sectional
Participants79
Evidence strengthLow

How this study scored 55/100

Published in a leading specialty 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	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	4 / 12	A snapshot of people at one point in time
Strength of evidence	1 / 5	Rated “low” in our summary
Peer-review validation	10 / 10	Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent	2 / 5	2018 — within 10 year(s) of the newest study here
Sample size	1 / 4	79 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	4 / 7	Cited 49 times (OpenAlex, 2026-10-10)
Citations per year	2 / 5	4.9 citations a year over 10 year(s) since 2018
Impact for its field and year	3 / 6	Cited 5.0× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here	2 / 6	Cited by 3 other studies in this library
Still being cited	1 / 4	Cited 10 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Barbara B. Bendlin: h-index 64 (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 9 institution(s) in 3 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 29959263)
Free to read	0 / 2	Behind a paywall — scores zero
Total	55 / 100	—

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