The University of Southampton
University of Southampton Institutional Repository

Targeting microglial population dynamics in Alzheimer’s disease: are we ready for a potential impact on immune function?

Targeting microglial population dynamics in Alzheimer’s disease: are we ready for a potential impact on immune function?
Targeting microglial population dynamics in Alzheimer’s disease: are we ready for a potential impact on immune function?
Alzheimer’s disease (AD) is the most common form of dementia, affecting two-thirds of people with dementia in the world. To date, no disease-modifying treatments are available to stop or delay the progression of AD. This chronic neurodegenerative disease is dominated by a strong innate immune response, whereby microglia plays a central role as the main resident macrophage of the brain. Recent genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) located in microglial genes and associated with a delayed onset of AD, highlighting the important role of these cells on the onset and/or progression of the disease. These findings have increased the interest in targeting microglia-associated neuroinflammation as a potential disease-modifying therapeutic approach for AD. In this review we provide an overview on the contribution of microglia to the pathophysiology of AD, focusing on the main regulatory pathways controlling microglialdynamics during the neuroinflammatory response, such as the colony-stimulating factor 1 receptor (CSF1R), its ligands (the colony stimulating factor 1and interleukin 34) and the transcription factor PU.1. We also discuss the current therapeutic strategies targeting proliferationto modulate microglia-associated neuroinflammation and their potential impact on peripheral immune cell populations in the short and long-term. Understanding the effects ofimmunomodulatory approaches on microglia and other immune cell types might be critical for developing specific, effective and safe therapies for neurodegenerative diseases.
1662-5102
Martin Estebane, Maria
51e238f8-2ae3-4914-8e84-71f09e6b4f58
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5
Martin Estebane, Maria
51e238f8-2ae3-4914-8e84-71f09e6b4f58
Gomez-Nicola, Diego
0680aa66-9dee-47cf-a8d3-e39c988f85b5

Martin Estebane, Maria and Gomez-Nicola, Diego (2020) Targeting microglial population dynamics in Alzheimer’s disease: are we ready for a potential impact on immune function? Frontiers in Cellular Neuroscience. (In Press)

Record type: Review

Abstract

Alzheimer’s disease (AD) is the most common form of dementia, affecting two-thirds of people with dementia in the world. To date, no disease-modifying treatments are available to stop or delay the progression of AD. This chronic neurodegenerative disease is dominated by a strong innate immune response, whereby microglia plays a central role as the main resident macrophage of the brain. Recent genome-wide association studies (GWASs) have identified single-nucleotide polymorphisms (SNPs) located in microglial genes and associated with a delayed onset of AD, highlighting the important role of these cells on the onset and/or progression of the disease. These findings have increased the interest in targeting microglia-associated neuroinflammation as a potential disease-modifying therapeutic approach for AD. In this review we provide an overview on the contribution of microglia to the pathophysiology of AD, focusing on the main regulatory pathways controlling microglialdynamics during the neuroinflammatory response, such as the colony-stimulating factor 1 receptor (CSF1R), its ligands (the colony stimulating factor 1and interleukin 34) and the transcription factor PU.1. We also discuss the current therapeutic strategies targeting proliferationto modulate microglia-associated neuroinflammation and their potential impact on peripheral immune cell populations in the short and long-term. Understanding the effects ofimmunomodulatory approaches on microglia and other immune cell types might be critical for developing specific, effective and safe therapies for neurodegenerative diseases.

Text
Ms NI and AD-final revised version 2 - Accepted Manuscript
Available under License Creative Commons Attribution.
Download (501kB)

More information

Accepted/In Press date: 5 May 2020

Identifiers

Local EPrints ID: 440682
URI: http://eprints.soton.ac.uk/id/eprint/440682
ISSN: 1662-5102
PURE UUID: 108af4a4-a3c6-42e1-8b4b-067167c07979
ORCID for Diego Gomez-Nicola: ORCID iD orcid.org/0000-0002-5316-2682

Catalogue record

Date deposited: 13 May 2020 16:35
Last modified: 07 Oct 2020 01:58

Export record

Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton: eprints@soton.ac.uk

ePrints Soton supports OAI 2.0 with a base URL of http://eprints.soton.ac.uk/cgi/oai2

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.

×