Targeting neuroinflammation in Alzheimer’s disease

Targeting neuroinflammation in Alzheimer’s disease

Maria Rosanna Bronzuoli,1 Aniello Iacomino,2 Luca Steardo,1 Caterina Scuderi1 1Department of Physiology and Pharmacology “Vittorio Erspamer”, Sapienza University of Rome, Rome, Italy; 2Faculty of Psychology, University of Rome “G. Marconi”, Rome, Italy Abstrac...

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Autores principales: Bronzuoli MR, Iacomino A, Steardo L, Scuderi C
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2016
Materias:
Neuroinflammation
Astrocyte
Microglia
Alzheimer’s disease
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
Acceso en línea:https://doaj.org/article/966a28324cd842ec8cf572845128efa6
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spelling oai:doaj.org-article:966a28324cd842ec8cf572845128efa62021-12-02T06:38:14ZTargeting neuroinflammation in Alzheimer’s disease1178-7031https://doaj.org/article/966a28324cd842ec8cf572845128efa62016-11-01T00:00:00Zhttps://www.dovepress.com/targeting-neuroinflammation-in-alzheimerrsquos-disease-peer-reviewed-article-JIRhttps://doaj.org/toc/1178-7031Maria Rosanna Bronzuoli,1 Aniello Iacomino,2 Luca Steardo,1 Caterina Scuderi1 1Department of Physiology and Pharmacology “Vittorio Erspamer”, Sapienza University of Rome, Rome, Italy; 2Faculty of Psychology, University of Rome “G. Marconi”, Rome, Italy Abstract: 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. Keywords: reactive gliosis, astrocyte, microglia, Alzheimer’s diseaseBronzuoli MRIacomino ASteardo LScuderi CDove Medical PressarticleNeuroinflammationAstrocyteMicrogliaAlzheimer’s diseasePathologyRB1-214Therapeutics. PharmacologyRM1-950ENJournal of Inflammation Research, Vol Volume 9, Pp 199-208 (2016)
institution DOAJ
collection DOAJ
language EN
topic Neuroinflammation
Astrocyte
Microglia
Alzheimer’s disease
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
spellingShingle Neuroinflammation
Astrocyte
Microglia
Alzheimer’s disease
Pathology
RB1-214
Therapeutics. Pharmacology
RM1-950
Bronzuoli MR
Iacomino A
Steardo L
Scuderi C
Targeting neuroinflammation in Alzheimer’s disease
description Maria Rosanna Bronzuoli,1 Aniello Iacomino,2 Luca Steardo,1 Caterina Scuderi1 1Department of Physiology and Pharmacology “Vittorio Erspamer”, Sapienza University of Rome, Rome, Italy; 2Faculty of Psychology, University of Rome “G. Marconi”, Rome, Italy Abstract: 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. Keywords: reactive gliosis, astrocyte, microglia, Alzheimer’s disease
format article
author Bronzuoli MR
Iacomino A
Steardo L
Scuderi C
author_facet Bronzuoli MR
Iacomino A
Steardo L
Scuderi C
author_sort Bronzuoli MR
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
publisher Dove Medical Press
publishDate 2016
url https://doaj.org/article/966a28324cd842ec8cf572845128efa6
work_keys_str_mv AT bronzuolimr targetingneuroinflammationinalzheimerrsquosdisease
AT iacominoa targetingneuroinflammationinalzheimerrsquosdisease
AT steardol targetingneuroinflammationinalzheimerrsquosdisease
AT scuderic targetingneuroinflammationinalzheimerrsquosdisease
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