Evidence mapPaperPMID 40140971Full record

ReviewExpert review of neurotherapeutics2025

Cholesterol-modifying strategies for Alzheimer disease: promise or fallacy?

Katia Azarfar, Boris Decourt, Brandon Sanchez Camacho, John Joshua Lawrence, Tania R Omondi, Marwan N Sabbagh

Abstract readReview
In one paragraph

Review in Expert review of neurotherapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Katia AzarfarDepartment of Pharmacology and Neurosciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Boris DecourtDepartment of Pharmacology and Neurosciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Brandon Sanchez CamachoDepartment of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.
John Joshua LawrenceDepartment of Pharmacology and Neurosciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Tania R OmondiDepartment of Pharmacology and Neurosciences, Texas Tech University Health Sciences Center, Lubbock, TX, USA.
Marwan N SabbaghDepartment of Neurosurgery, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, AZ, USA.

Funding

Research Education ComponentP30AG072980 · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · 2025 to 2025
$3.1M
Repurposing Siponimod for Alzheimer's DiseaseR01AG073212 · NIA · ST. JOSEPH'S HOSPITAL AND MEDICAL CENTER · PI Boris Decourt, MARWAN Noel SABBAGH · 2023 to 2023
$687k
Assessment of lenalidomide to treat Alzheimer's diseaseR01AG059008 · NIA · CLEVELAND CLINIC LERNER COM-CWRU · PI Boris Decourt, MARWAN Noel SABBAGH · 2021 to 2021
$640k
NIA NIH HHS P30 AG072980NIA NIH HHS R01 AG059008NIA NIH HHS R01 AG073212
6 · The paper itself

Abstract

introductionAs the world population ages, Alzheimer disease (AD) prevalence increases. However, understanding of AD etiology continues to evolve, and the pathophysiological processes involved are only partially elucidated. One compound suspected to play a role in the development and progression of AD is cholesterol. Several lines of evidence support this connection, yet it remains unclear whether cholesterol-modifying strategies have potential applications in the clinical management of AD. AREAS COVERED: A deep literature search using PubMed was performed to prepare this narrative review. The literature search, performed in early 2024, was inclusive of literature from 1990 to 2024. After providing an overview of cholesterol metabolism, this study summarizes key preclinical studies that have investigated cholesterol-modifying therapies in laboratory models of AD. It also summarizes past and current clinical trials testing specific targets modulated by anti-cholesterol therapies in AD patients. EXPERT OPINION: Based on current epidemiological and mechanistic studies, cholesterol likely plays a role in AD etiology. The use of cholesterol-modifying therapies could be a promising treatment approach if administered at presymptomatic to early AD phases, but it is unlikely to be efficient in mild, moderate, and late AD stages. Several recommendations are provided for hypercholesterolemia management in AD patients.

Indexed as

Alzheimer DiseaseAnticholesteremic AgentsCholesterolAnimalsHumansAnticholesteremic AgentsCholesterolAlzheimer diseaseamyloid betaastrocytescholesterolclinical trialsdementianeuronsstatins

Identifiers

PMID40140971
PMCPMC12068190

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.