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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 35 out of 100. Biomarkers

Topic: Brain proteins, microglia and lab models

Brain spectrin is a major membrane skeleton protein that participates in cellular transport, cell morphogenesis, neurotransmitter release and growth cone adhesion. The present study showed that in Alzheimer disease (AD) neuropil, brain spectrin immunoreactivity is co-localized with synaptophysin in the presynaptic boutons. At the ultrastructural level, brain spectrin immunoreactivity was observed in the presynaptic terminals and in the axoplasm of some myelinated and unmyelinated fibers. In addition to this normal localization of brain spectrin in the AD brain, we also found brain spectrin immunoreactivity associated with abnormal patchy lesions in the AD neuropil. Confocal laser imaging and immunoelectron microscopy revealed that these lesions corresponded to thick cellular processes derived from neurons. The findings that these structures were anti-neurofilament positive but anti-glial fibrillary acidic protein (GFAP) and Ricinus communis agglutinin I (RCA-I) negative confirm their neuronal origin, and rule out the possibility of glial origin. These structures could represent either atypical axonal or dendritic processes derived from sprouting neurons or the accumulation of brain spectrin degradation products in degenerating neurons.

Key findings

Why it matters

This study found abnormal brain spectrin immunoreactivity in neuronal processes in Alzheimer's disease brain tissue, possibly from sprouting neurons or degeneration products. It is a descriptive pathology study and does not test any treatment, cure, or prevention for Alzheimer's disease.

Study details

How this study scored 35/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 3 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 1 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 3 of 7; Citations per year 0 of 5; Impact for its field and year 2 of 6; Cited by studies here 0 of 6; Still being cited 0 of 4; Senior author's track record 3 of 4; Institution's track record 2 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 35 of 100.35 of 100 points earned65 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Neuroscience letters)
Journal's citation record 3 / 4 Neuroscience Letters: journal h-index 267 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
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 1 / 5 1991 — older than 20 years, still counted
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 3 / 7 Cited 33 times (OpenAlex, 2026-10-10)
Citations per year 0 / 5 0.9 citations a year over 37 year(s) since 1991
Impact for its field and year 2 / 6 Cited 1.2× 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 3 / 4 Last-listed author Robert D. Terry: h-index 75 (OpenAlex, whole career)
Institution's track record 2 / 3 University of California San Diego: institution h-index 1,852 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 1 country
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 1922957)
Free to read 0 / 2 Behind a paywall — scores zero
Total 35 / 100 —

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

Read the original

May need a subscription Unpaywall, Europe PMC and OpenAlex found no free copy of the full text (checked 10 Oct 2026), so the publisher may charge for it. The PubMed abstract is free.

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

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Masliah, E., Hansen, L., Mallory, M., Albright, T., & Terry, R. D. (1991). Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease. Neuroscience letters. https://doi.org/10.1016/0304-3940(91)90707-z

Vancouver

Masliah E, Hansen L, Mallory M, Albright T, Terry RD. Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease. Neuroscience letters. 1991. doi:10.1016/0304-3940(91)90707-z. PMID: 1922957.

BibTeX

@article{masliah1991-1922957,
  author  = {Masliah, E. and Hansen, L. and Mallory, M. and Albright, T. and Terry, R. D.},
  title   = {{Abnormal brain spectrin immunoreactivity in sprouting neurons in Alzheimer disease}},
  journal = {Neuroscience letters},
  year    = {1991},
  doi     = {10.1016/0304-3940(91)90707-z},
  pmid    = {1922957},
  url     = {https://doi.org/10.1016/0304-3940(91)90707-z}
}

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