Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

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 39 out of 100. Biomarkers

Topic: Brain proteins, microglia and lab models

Proteins relatively enriched in neurons (neural cell adhesion molecule (NCAM) and D3-protein) or in glia (glutamine synthetase, glial fibrillary acidic protein (GFAP) and S100) were measured by quantitative immunochemical methods in autopsy samples of the cerebral cortex of subjects with Alzheimer disease (AD) and adults with Down syndrome (DS), the latter also presenting manifest signs of Alzheimer type of neuropathology. The trend of changes was similar in AD and DS, but more marked in the latter. The biochemical make-up of astrocytes was differentially affected: in both the frontal and DS temporal cortex the specific concentration of glutamine synthetase was unaltered, while that of S100 and the soluble form of GFAP was markedly elevated (about 260% and 690% of control values, respectively). In the AD frontal cortex the estimates for glutamine synthetase were normal, while S100 and GFAP were about 180% and 230% of control. The observations (normal GS and elevated levels of the other markers) might suggest that the pathological changes involve a differentiated astrocytic reaction and that the astrocytic reaction is more marked in DS than in AD. In DS the increase in S100 could be explained, in part, by a gene dosage effect and in part by reactive gliosis. The neuronal markers were also differentially affected. In comparison with appropriate controls, the concentration of D3-protein in frontal cortex was decreased by 24% in DS and by 14% in AD, whereas NCAM levels were not significantly affected. The ratio of NCAM to D3-protein was significantly increased by 32% and 8.5% in DS and AD, respectively. These observations are consistent with the view that the destruction of mature neuronal structures (as marked by the D-3 protein) coincides with the formation of new neuronal membranes (as indicated by NCAM), i.e. in these degenerative disorders plastic changes are taking place involving cerebral cortex neurons in which trophic substances may be instrumental.

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

APA 7th

Jørgensen, O. S., Brooksbank, B. W., & Balázs, R. (1990). Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. Journal of the neurological sciences. https://doi.org/10.1016/0022-510x(90)90182-m

Vancouver

Jørgensen OS, Brooksbank BW, Balázs R. Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease. Journal of the neurological sciences. 1990. doi:10.1016/0022-510x(90)90182-m. PMID: 1977892.

BibTeX

@article{jorgensen1990-1977892,
  author  = {Jørgensen, O. S. and Brooksbank, B. W. and Balázs, R.},
  title   = {{Neuronal plasticity and astrocytic reaction in Down syndrome and Alzheimer disease}},
  journal = {Journal of the neurological sciences},
  year    = {1990},
  doi     = {10.1016/0022-510x(90)90182-m},
  pmid    = {1977892},
  url     = {https://doi.org/10.1016/0022-510x(90)90182-m}
}

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.

Key findings

Why it matters

This autopsy study compared brain proteins in people with Alzheimer's disease and adults with Down syndrome, finding a more marked astrocytic reaction in Down syndrome. It is a tissue study and does not test any treatment, cure or prevention.

Study details

How this study scored 39/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 2 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 2 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 4 of 7; Citations per year 1 of 5; Impact for its field and year 2 of 6; Cited by studies here 2 of 6; Still being cited 1 of 4; Senior author's track record 3 of 4; Institution's track record 1 of 3; Multi-centre collaboration 0 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 39 of 100.39 of 100 points earned61 not earned

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

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Journal of the neurological sciences)
Journal's citation record 2 / 4 Journal of the Neurological Sciences: journal h-index 233 (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 1990 — 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 2 / 3 Effect reported as a number, without an interval or test
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 4 / 7 Cited 99 times (OpenAlex, 2026-10-10)
Citations per year 1 / 5 2.6 citations a year over 38 year(s) since 1990
Impact for its field and year 2 / 6 Cited 2.8× 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 6 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author R. Balázs: h-index 55 (OpenAlex, whole career)
Institution's track record 1 / 3 University of Copenhagen: institution h-index 1,378 (OpenAlex)
Multi-centre collaboration 0 / 3 OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete)
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 1977892)
Free to read 0 / 2 Behind a paywall — scores zero
Total 39 / 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.

Studies this one cites

Referenced by this study and also in the alzhub library, so you can read them here.

Later studies that cite this one

3 studies in the alzhub library list this one in their references.

Related studies in Biomarkers

Also tagged “down”

527 studies in the library carry the topic tag “down”; these are this study's neighbours in a fixed, alphabetical-by-hash tour of them, not the closest in content. All 527 tagged studies.

Similar studies

More on Biomarkers

See all studies in Biomarkers →