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36/100

✓ Peer-reviewed alzhub usefulness score 36 out of 100. Drug development

Topic: Amyloid, tau and blood-test diagnosis

Plain-language summary

The discovery that the apolipoprotein E4 (apoE4) allele is genetically linked to both sporadic and familial late onset Alzheimer's disease (AD) raises the possibility that a dysfunction of the lipid transport system could seriously affect lipid homeostasis in the brain of AD subjects. The presence of the E4 allele has been associated with lower levels of apoE in both serum and brain tissues of normal and AD subjects. In an attempt to reverse the apoE deficit in AD, we identified and characterized several apoE inducer agents using a low throughput-screening assay. The most promising of these compounds is called probucol. Administration of probucol, an old cholesterol lowering drug, in mild to moderate sporadic AD led to significant increases in CSF apoE levels and a decrease of CSF beta amyloid 1-42 without significant modifications of CSF tau concentration or CSF lipid peroxides levels. These results are consistent with recent reports suggesting that the long term use of cholesterol lowering drugs that block 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity in the fourth and fifth decade of life may help reduce the risk of developing AD at later age. These results indicate that, in addition to lipid transport mediated by apoE, cholesterol homeostasis in the brain is markedly altered in response to changes in the HMGR pathway; suggesting a possible explanation for the potentially beneficial effect of statins in common AD.

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

APA 7th

Poirier, J. (2005). Apolipoprotein E, cholesterol transport and synthesis in sporadic Alzheimer's disease. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2004.09.003

Vancouver

Poirier J. Apolipoprotein E, cholesterol transport and synthesis in sporadic Alzheimer's disease. Neurobiology of aging. 2005. doi:10.1016/j.neurobiolaging.2004.09.003. PMID: 15639314.

BibTeX

@article{poirier2005-15639314,
  author  = {Poirier, J.},
  title   = {{Apolipoprotein E, cholesterol transport and synthesis in sporadic Alzheimer's disease}},
  journal = {Neurobiology of aging},
  year    = {2005},
  doi     = {10.1016/j.neurobiolaging.2004.09.003},
  pmid    = {15639314},
  url     = {https://doi.org/10.1016/j.neurobiolaging.2004.09.003}
}

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How to read this study

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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

The presence of the E4 allele has been associated with lower levels of apoE in both serum and brain tissues of normal and AD subjects.
Administration of probucol, an old cholesterol lowering drug, in mild to moderate sporadic AD led to significant increases in CSF apoE levels and a decrease of CSF beta amyloid 1-42 without significant modifications of CSF tau concentration or CSF lipid peroxides levels.
These results are consistent with recent reports suggesting that the long term use of cholesterol lowering drugs that block 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGR) activity in the fourth and fifth decade of life may help reduce the risk of developing AD at later age.
These results indicate that, in addition to lipid transport mediated by apoE, cholesterol homeostasis in the brain is markedly altered in response to changes in the HMGR pathway; suggesting a possible explanation for the potentially beneficial effect of statins in common AD.

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Study details

Evidence strengthLow

How this study scored 36/100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people 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 21 of the 58 points we could judge it on, which is 36 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	2005 — 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)
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 15639314)
Free to read	0 / 2	Behind a paywall — scores zero
Points	21 / 58	Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 21 of the 58 points we could judge it on is 36 out of 100.
Total	36 / 100	—

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