7‐Keto Cholesterol as a Mediator in Alzheimer's Disease Pathogenesis

Irundika HK Dias; Lorena Diaz Sanchez; Tommaso Angelini; Maura Marinozzi

doi:10.1002/alz70856_105279

7‐Keto Cholesterol as a Mediator in Alzheimer's Disease Pathogenesis

Irundika HK Dias
, Lorena Diaz Sanchez
, Tommaso Angelini
, Maura Marinozzi

Galatasaray University, Istanbul, Türkiye#African Mathematical Union#Springer Nature Switzerland AG, Switzerland#The University of Massachusetts, USA#University of Perugia, Italy#University of Basilicata, Italy#Monash University, Australia#Kyushu Sangyo University, Japan#

Research output: Chapter in Book/Published conference output › Conference publication

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Abstract

Background

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and oxidative stress. Recent evidence suggests that oxysterols, particularly 7-ketocholesterol (7-KC) may play a pivotal role in AD pathology by exacerbating neuroinflammatory and oxidative damage. 7-KC, a major non-enzymatic oxidation product of cholesterol, is known to contribute to neurotoxicity through mitochondrial dysfunction, lipid peroxidation, and inflammation. Unlike other oxysterols, 7-KC is highly reactive and has been implicated in cell death pathways relevant to neurodegeneration, including ferroptosis and autophagy dysregulation. Sulphation of 7-KC alter its solubility, bioavailability, and interaction with cellular receptors, potentially amplifying its cytotoxic effects in neuronal and glial cells.

Original language	English
Title of host publication	Alzheimer's & Dementia
Publisher	Wiley
Number of pages	1
Volume	21
Edition	S2
DOIs	https://doi.org/10.1002/alz70856_105279 https://doi.org/10.1002/alz.v21.S2
Publication status	Published - 7 Jan 2026

Publication series

Name	Alzheimer's & Dementia
Publisher	Wiley-Blackwell
ISSN (Print)	1552-5260

Bibliographical note

This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided
the original work is properly cited.

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10.1002/alz70856_105279Licence: CC BY 3.0
10.1002/alz.v21.S2Licence: CC BY 4.0

Alzheimer s Dementia - 2026 - Dias - 7‐Keto Cholesterol as a Mediator in Alzheimer s Disease Pathogenesis
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
Final published version, 77.2 KBLicence: CC BY 4.0

Cite this

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title = "7‐Keto Cholesterol as a Mediator in Alzheimer's Disease Pathogenesis",

abstract = "Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and oxidative stress. Recent evidence suggests that oxysterols, particularly 7-ketocholesterol (7-KC) may play a pivotal role in AD pathology by exacerbating neuroinflammatory and oxidative damage. 7-KC, a major non-enzymatic oxidation product of cholesterol, is known to contribute to neurotoxicity through mitochondrial dysfunction, lipid peroxidation, and inflammation. Unlike other oxysterols, 7-KC is highly reactive and has been implicated in cell death pathways relevant to neurodegeneration, including ferroptosis and autophagy dysregulation. Sulphation of 7-KC alter its solubility, bioavailability, and interaction with cellular receptors, potentially amplifying its cytotoxic effects in neuronal and glial cells.",

author = "Dias, \{Irundika HK\} and \{Diaz Sanchez\}, Lorena and Tommaso Angelini and Maura Marinozzi",

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AU - Dias, Irundika HK

AU - Diaz Sanchez, Lorena

AU - Angelini, Tommaso

AU - Marinozzi, Maura

N1 - This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

PY - 2026/1/7

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N2 - Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and oxidative stress. Recent evidence suggests that oxysterols, particularly 7-ketocholesterol (7-KC) may play a pivotal role in AD pathology by exacerbating neuroinflammatory and oxidative damage. 7-KC, a major non-enzymatic oxidation product of cholesterol, is known to contribute to neurotoxicity through mitochondrial dysfunction, lipid peroxidation, and inflammation. Unlike other oxysterols, 7-KC is highly reactive and has been implicated in cell death pathways relevant to neurodegeneration, including ferroptosis and autophagy dysregulation. Sulphation of 7-KC alter its solubility, bioavailability, and interaction with cellular receptors, potentially amplifying its cytotoxic effects in neuronal and glial cells.

AB - Background Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and oxidative stress. Recent evidence suggests that oxysterols, particularly 7-ketocholesterol (7-KC) may play a pivotal role in AD pathology by exacerbating neuroinflammatory and oxidative damage. 7-KC, a major non-enzymatic oxidation product of cholesterol, is known to contribute to neurotoxicity through mitochondrial dysfunction, lipid peroxidation, and inflammation. Unlike other oxysterols, 7-KC is highly reactive and has been implicated in cell death pathways relevant to neurodegeneration, including ferroptosis and autophagy dysregulation. Sulphation of 7-KC alter its solubility, bioavailability, and interaction with cellular receptors, potentially amplifying its cytotoxic effects in neuronal and glial cells.

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M3 - Conference publication

VL - 21

T3 - Alzheimer's & Dementia

BT - Alzheimer's & Dementia

PB - Wiley

ER -

7‐Keto Cholesterol as a Mediator in Alzheimer's Disease Pathogenesis

Abstract

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