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41/100

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Genetics

Topic: Brain imaging, connectivity and assessment

Plain-language summary

One of the major neuropathological findings in the brains of individuals with Alzheimer's disease (AD) is a loss of synaptic contacts in both the neocortex and hippocampus. Here we report, for the first time, an estimate of the total number of synapses in the outer molecular layer (OML) of the human dentate gyrus, in individuals with early Alzheimer's disease (eAD), mild cognitive impairment (MCI), or no cognitive impairment (NCI). An unbiased stereologic sampling scheme coupled with transmission electron microscopy to directly visualize synaptic contacts, was used to estimate the total number of synapses in short postmortem autopsy tissue. Individuals with eAD had significantly fewer synapses than the other two diagnostic groups. Seventy-five percent of the individuals with MCI had synaptic values that were lower than the NCI group mean. The number of synapses showed a significant correlation with the subject's Mini-Mental State score and with cognitive tests involving delayed recall. Synaptic loss showed no relationship to Braak stage or to apoE genotype. The volume of the OML was significantly reduced in eAD compared to the other two diagnositic groups that were not different from each other. These data suggest that a loss of afferents from the entorhinal cortex underlie the synapse loss seen in eAD. This study supports the concept that synapse loss is an early event in the disease process and suggests that MCI may be a transition stage between eAD and NCI with synaptic loss a structural correlate involved in cognitive decline.

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

APA 7th

Scheff, S. W., Price, D. A., Schmitt, F. A., & Mufson, E. J. (2006). Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2005.09.012

Vancouver

Scheff SW, Price DA, Schmitt FA, Mufson EJ. Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment. Neurobiology of aging. 2006. doi:10.1016/j.neurobiolaging.2005.09.012. PMID: 16289476.

BibTeX

@article{scheff2006-16289476,
  author  = {Scheff, S. W. and Price, D. A. and Schmitt, F. A. and Mufson, E. J.},
  title   = {{Hippocampal synaptic loss in early Alzheimer's disease and mild cognitive impairment}},
  journal = {Neurobiology of aging},
  year    = {2006},
  doi     = {10.1016/j.neurobiolaging.2005.09.012},
  pmid    = {16289476},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2005.09.012}
}

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How to read this study

Design: this is a trial. Participants are assigned to a treatment or a comparison, so the key questions are who was enrolled, whether the comparison group got a placebo or nothing, how long people were followed, and whether the result is on a measure that matters to patients or on a biomarker. Open-label and small trials can overstate benefit.
Size: the record gives no participant count. Look for one in the original before trusting a pattern.
Effect: the record gives no effect size, so the summary above cannot say how large any difference was.

What the evidence grade means here

This page is graded low. alzhub.org assigns the grade automatically from keywords in the abstract, not from reading the paper. Low means the abstract matched neither pattern. It is the default label, and it does not mean the work is poor; many sound lab and imaging papers land here. It can add at most 5 of the 100 points in the study score, and it is a label about design, not a verdict on whether the findings are true.

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Key findings

Individuals with eAD had significantly fewer synapses than the other two diagnostic groups.
The number of synapses showed a significant correlation with the subject's Mini-Mental State score and with cognitive tests involving delayed recall.
The volume of the OML was significantly reduced in eAD compared to the other two diagnositic groups that were not different from each other.
These data suggest that a loss of afferents from the entorhinal cortex underlie the synapse loss seen in eAD.
This study supports the concept that synapse loss is an early event in the disease process and suggests that MCI may be a transition stage between eAD and NCI with synaptic loss a structural correlate involved in cognitive decline.

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Study details

Evidence strengthLow

How this study scored 41/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomized / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multicenter collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Neurobiology of aging)
Journal's citation record	— / 4	No journal record from OpenAlex — left out of this score
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	2006 — 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	3 / 3	Studied in people (pubmed indexes it as a clinical or observational study)
Randomized / blinded	0 / 2	No randomization or blinding stated — scores zero (not stated in the record — scored 0)
Times cited	— / 7	No citation count (not found in OpenAlex) — left out of this score
Citations per year	— / 5	No citation count or no year — left out of this score
Impact for its field and year	— / 6	No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here	— / 6	Not yet checked against this library's citation graph — left out of this score
Still being cited	— / 4	No yearly citation counts — left out of this score
Senior author's track record	— / 4	Senior author's record not available — left out of this score
Institution's track record	— / 3	No institution listed in OpenAlex — left out of this score
Multicenter collaboration	— / 3	Institutions not listed — left out of this score
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 16289476)
Free to read	0 / 2	Behind a paywall — scores zero
Points	24 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100.
Total	41 / 100	—

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

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