Targeting neuroinflammation in Alzheimer’s disease

Almost 47 million people suffer from dementia worldwide, with an estimated new case diagnosed every 3.2 seconds. Alzheimer’s disease (AD) accounts for approximately 60%–80% of all dementia cases. Given this evidence, it is clear dementia represents one of the greatest global public health challenges...

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Main Authors:	Bronzuoli, Maria Rosanna, Iacomino, Aniello, Steardo, Luca, Scuderi, Caterina
Format:	Online
Language:	English
Published:	Dove Medical Press 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098782/

id	pubmed-5098782
recordtype	oai_dc
spelling	pubmed-50987822016-11-14 Targeting neuroinflammation in Alzheimer’s disease Bronzuoli, Maria Rosanna Iacomino, Aniello Steardo, Luca Scuderi, Caterina Review Almost 47 million people suffer from dementia worldwide, with an estimated new case diagnosed every 3.2 seconds. Alzheimer’s disease (AD) accounts for approximately 60%–80% of all dementia cases. Given this evidence, it is clear dementia represents one of the greatest global public health challenges. Currently used drugs alleviate the symptoms of AD but do not treat the underlying causes of dementia. Hence, a worldwide quest is under way to find new treatments to stop, slow, or even prevent AD. Besides the classic targets of the oldest therapies, represented by cholinergic and glutamatergic systems, β-amyloid (Aβ) plaques, and tau tangles, new therapeutic approaches have other targets. One of the newest and most promising strategies is the control of reactive gliosis, a multicellular response to brain injury. This phenomenon occurs as a consequence of a persistent glial activation, which leads to cellular dysfunctions and neuroinflammation. Reactive gliosis is now considered a key abnormality in the AD brain. It has been demonstrated that reactive astrocytes surround both Aβ plaques and tau tangles. In this condition, glial cells lose some of their homeostatic functions and acquire a proinflammatory phenotype amplifying neuronal damage. So, molecules that are able to restore their physiological functions and control the neuroinflammatory process offer new therapeutic opportunities for this devastating disease. In this review, we describe the role of neuroinflammation in the AD pathogenesis and progression and then provide an overview of the recent research with the aim of developing new therapies to treat this disorder. Dove Medical Press 2016-11-03 /pmc/articles/PMC5098782/ /pubmed/27843334 http://dx.doi.org/10.2147/JIR.S86958 Text en © 2016 Bronzuoli et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Bronzuoli, Maria Rosanna Iacomino, Aniello Steardo, Luca Scuderi, Caterina
spellingShingle	Bronzuoli, Maria Rosanna Iacomino, Aniello Steardo, Luca Scuderi, Caterina Targeting neuroinflammation in Alzheimer’s disease
author_facet	Bronzuoli, Maria Rosanna Iacomino, Aniello Steardo, Luca Scuderi, Caterina
author_sort	Bronzuoli, Maria Rosanna
title	Targeting neuroinflammation in Alzheimer’s disease
title_short	Targeting neuroinflammation in Alzheimer’s disease
title_full	Targeting neuroinflammation in Alzheimer’s disease
title_fullStr	Targeting neuroinflammation in Alzheimer’s disease
title_full_unstemmed	Targeting neuroinflammation in Alzheimer’s disease
title_sort	targeting neuroinflammation in alzheimer’s disease
description	Almost 47 million people suffer from dementia worldwide, with an estimated new case diagnosed every 3.2 seconds. Alzheimer’s disease (AD) accounts for approximately 60%–80% of all dementia cases. Given this evidence, it is clear dementia represents one of the greatest global public health challenges. Currently used drugs alleviate the symptoms of AD but do not treat the underlying causes of dementia. Hence, a worldwide quest is under way to find new treatments to stop, slow, or even prevent AD. Besides the classic targets of the oldest therapies, represented by cholinergic and glutamatergic systems, β-amyloid (Aβ) plaques, and tau tangles, new therapeutic approaches have other targets. One of the newest and most promising strategies is the control of reactive gliosis, a multicellular response to brain injury. This phenomenon occurs as a consequence of a persistent glial activation, which leads to cellular dysfunctions and neuroinflammation. Reactive gliosis is now considered a key abnormality in the AD brain. It has been demonstrated that reactive astrocytes surround both Aβ plaques and tau tangles. In this condition, glial cells lose some of their homeostatic functions and acquire a proinflammatory phenotype amplifying neuronal damage. So, molecules that are able to restore their physiological functions and control the neuroinflammatory process offer new therapeutic opportunities for this devastating disease. In this review, we describe the role of neuroinflammation in the AD pathogenesis and progression and then provide an overview of the recent research with the aim of developing new therapies to treat this disorder.
publisher	Dove Medical Press
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5098782/
_version_	1613716299351851008

Targeting neuroinflammation in Alzheimer’s disease

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