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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 49 out of 100. Mild cognitive impairment

Topic: Amyloid, tau and blood-test diagnosis

Nerve growth factor (NGF) is critical for the regulation, differentiation, and survival of basal forebrain cholinergic neurons that degenerate in the late stage of Alzheimer disease (AD). The precursor of NGF (proNGF) is the predominant form of NGF in brain and is increased in end stage AD. To determine whether this increase in proNGF is an early or late change during the progression of cognitive decline, we used Western blotting to measure the relative amounts of proNGF protein in the parietal cortex from subjects clinically classified with no cognitive impairment (NCI; n = 20), mild cognitive impairment (MCI; n = 20), or mild to moderate AD (n = 19). We found that proNGF increased during the prodromal stage of AD. The amount of proNGF protein was 1.4-fold greater in the MCI group as compared to NCI, and was 1.6-fold greater in mild-moderate AD as compared to NCI, similar to our previous findings of a 2-fold increase in end stage AD. There was a negative correlation between proNGF levels and Mini Mental Status Examination (MMSE) score, demonstrating that the accumulation of proNGF is correlated with loss of cognitive function. These findings demonstrate that proNGF levels increase during the preclinical stage of AD and may reflect an early biological marker for the onset of AD.

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

APA 7th

Peng, S., Wuu, J., Mufson, E. J., & Fahnestock, M. (2004). Increased proNGF levels in subjects with mild cognitive impairment and mild Alzheimer disease. Journal of neuropathology and experimental neurology. https://doi.org/10.1093/jnen/63.6.641

Vancouver

Peng S, Wuu J, Mufson EJ, Fahnestock M. Increased proNGF levels in subjects with mild cognitive impairment and mild Alzheimer disease. Journal of neuropathology and experimental neurology. 2004. doi:10.1093/jnen/63.6.641. PMID: 15217092.

BibTeX

@article{peng2004-15217092,
  author  = {Peng, S. and Wuu, J. and Mufson, E. J. and Fahnestock, M.},
  title   = {{Increased proNGF levels in subjects with mild cognitive impairment and mild Alzheimer disease}},
  journal = {Journal of neuropathology and experimental neurology},
  year    = {2004},
  doi     = {10.1093/jnen/63.6.641},
  pmid    = {15217092},
  url     = {https://doi.org/10.1093/jnen/63.6.641}
}

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

In this study, proNGF protein was 1.4-fold greater in the mild cognitive impairment group and 1.6-fold greater in mild to moderate Alzheimer's disease compared with no cognitive impairment, and proNGF levels negatively correlated with Mini Mental Status Examination score. The authors suggest proNGF levels increase during the preclinical stage of Alzheimer's disease and may reflect an early biological marker, but no treatment was tested.

Study details

How this study scored 49/100
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 1 of 4; Effect reported 0 of 3; Studied in people 3 of 3; Randomised / blinded 0 of 2; Times cited 5 of 7; Citations per year 3 of 5; Impact for its field and year 4 of 6; Cited by studies here 3 of 6; Still being cited 2 of 4; Senior author's track record 3 of 4; Institution's track record 1 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 0 of 2. Total 49 of 100.49 of 100 points earned51 not earned

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

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Journal of neuropathology and experimental neurology)
Journal's citation record 2 / 4 Journal of Neuropathology & Experimental Neurology: journal h-index 239 (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 2004 — older than 20 years, still counted
Sample size 1 / 4 20 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 5 / 7 Cited 236 times (OpenAlex, 2026-10-10)
Citations per year 3 / 5 9.8 citations a year over 24 year(s) since 2004
Impact for its field and year 4 / 6 Cited 8.4× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 3 / 6 Cited by 10 other studies in this library
Still being cited 2 / 4 Cited 19 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 3 / 4 Last-listed author Margaret L. Fahnestock: h-index 58 (OpenAlex, whole career)
Institution's track record 1 / 3 McMaster University: institution h-index 1,334 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 15217092)
Free to read 0 / 2 Behind a paywall — scores zero
Total 49 / 100 —

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

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