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45/100

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Genetics

Topic: Amyloid, tau and blood-test diagnosis

Aberrant cholesterol metabolism has been implicated in Alzheimer disease (AD) and other neurological disorders. Oxysterols and other cholesterol oxidation products are effective ligands of liver X activated receptor (LXR) nuclear receptors, major regulators of genes subserving cholesterol homeostasis. LXR receptors act as molecular sensors of cellular cholesterol concentrations and effectors of tissue cholesterol reduction. Following their interaction with oxysterols, activation of LXRs induces the expression of ATP-binding cassette, sub-family A member 1, a pivotal modulator of cholesterol efflux. The relative solubility of oxysterols facilitates lipid flux among brain compartments and egress across the blood-brain barrier. Oxysterol-mediated LXR activation induces local apoE biosynthesis (predominantly in astrocytes) further enhancing cholesterol re-distribution and removal. Activated LXRs invoke additional neuroprotective mechanisms, including induction of genes governing bile acid synthesis (sterol elimination pathway), apolipoprotein elaboration, and amyloid precursor protein processing. The latter translates into attenuated beta-amyloid production that may ameliorate amyloidogenic neurotoxicity in AD brain. Stress-induced up-regulation of the heme-degrading enzyme, heme oxygenase-1 in AD-affected astroglia may impact central lipid homeostasis by promoting the oxidation of cholesterol to a host of oxysterol intermediates. Synthetic oxysterol-mimetic drugs that activate LXR receptors within the CNS may provide novel therapeutics for management of AD and other neurological afflictions characterized by deranged tissue cholesterol homeostasis.

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

APA 7th

Vaya, J., & Schipper, H. M. (2007). Oxysterols, cholesterol homeostasis, and Alzheimer disease. Journal of neurochemistry. https://doi.org/10.1111/j.1471-4159.2007.04689.x

Vancouver

Vaya J, Schipper HM. Oxysterols, cholesterol homeostasis, and Alzheimer disease. Journal of neurochemistry. 2007. doi:10.1111/j.1471-4159.2007.04689.x. PMID: 17573819.

BibTeX

@article{vaya2007-17573819,
  author  = {Vaya, J. and Schipper, H. M.},
  title   = {{Oxysterols, cholesterol homeostasis, and Alzheimer disease}},
  journal = {Journal of neurochemistry},
  year    = {2007},
  doi     = {10.1111/j.1471-4159.2007.04689.x},
  pmid    = {17573819},
  url     = {https://doi.org/10.1111/j.1471-4159.2007.04689.x}
}

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Key findings

Oxysterol-mediated LXR activation induces local apoE biosynthesis (predominantly in astrocytes) further enhancing cholesterol re-distribution and removal.
Activated LXRs invoke additional neuroprotective mechanisms, including induction of genes governing bile acid synthesis (sterol elimination pathway), apolipoprotein elaboration, and amyloid precursor protein processing.
The latter translates into attenuated beta-amyloid production that may ameliorate amyloidogenic neurotoxicity in AD brain.
Stress-induced up-regulation of the heme-degrading enzyme, heme oxygenase-1 in AD-affected astroglia may impact central lipid homeostasis by promoting the oxidation of cholesterol to a host of oxysterol intermediates.
Synthetic oxysterol-mimetic drugs that activate LXR receptors within the CNS may provide novel therapeutics for management of AD and other neurological afflictions characterized by deranged tissue cholesterol homeostasis.

Why it matters

This review describes how oxysterols activate LXR receptors, which regulate cholesterol homeostasis and can induce apoE production and reduce amyloid-beta production. It suggests that targeting cholesterol metabolism pathways may be a potential therapeutic approach, though this is a review of mechanisms rather than a clinical trial.

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Study details

Evidence strengthLow

How this study scored 45/100

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.

Component	Points	Why
Journal tier	7 / 10	Tier 3 — peer-reviewed journal (Journal of neurochemistry)
Journal's citation record	3 / 4	Journal of Neurochemistry: journal h-index 349 (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	2007 — within 20 year(s) of the newest study here
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	5 / 7	Cited 183 times (OpenAlex, 2026-10-10)
Citations per year	3 / 5	8.7 citations a year over 21 year(s) since 2007
Impact for its field and year	4 / 6	Cited 19.6× 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 9 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record	3 / 4	Last-listed author Hyman M. Schipper: h-index 58 (OpenAlex, whole career)
Institution's track record	1 / 3	McGill University: institution h-index 1,373 (OpenAlex)
Multicenter collaboration	2 / 3	OpenAlex lists 5 institution(s) in 2 countries
Indexed in PubMed	2 / 2	Indexed in PubMed (PMID 17573819)
Free to read	0 / 2	Behind a paywall — scores zero
Total	45 / 100	—

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