Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview

Neurodegenerative diseases are a group of disorders characterized by the progressive deterioration of the structure and function of central nervous system neurons and include, among others, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson’s (PD), Alzheimer’s (AD), and Huntingt...

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التفاصيل البيبلوغرافية
الحاوية / القاعدة:Pathophysiology
المؤلفون الرئيسيون: Judyta K. Juranek, Bernard Kordas, Piotr Podlasz, Agnieszka Bossowska, Marta Banach
التنسيق: مقال
اللغة:الإنجليزية
منشور في: MDPI AG 2025-08-01
الموضوعات:
الوصول للمادة أونلاين:https://www.mdpi.com/1873-149X/32/3/43
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author Judyta K. Juranek
Bernard Kordas
Piotr Podlasz
Agnieszka Bossowska
Marta Banach
author_facet Judyta K. Juranek
Bernard Kordas
Piotr Podlasz
Agnieszka Bossowska
Marta Banach
author_sort Judyta K. Juranek
collection DOAJ
container_title Pathophysiology
description Neurodegenerative diseases are a group of disorders characterized by the progressive deterioration of the structure and function of central nervous system neurons and include, among others, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson’s (PD), Alzheimer’s (AD), and Huntington’s (HD) diseases. And while all these diseases seem to have different genetic and environmental components, growing evidence shows that they share common underlying pathological features such as increased neuroinflammation and excessive oxidative stress. RAGE, the receptor for advanced glycation end-products, is a signal transduction receptor, and its activation triggers an increase in proinflammatory molecules, oxidative stressors, and cytokines. Diaph1, protein diaphanous homolog 1, is an actin modulator and an intracellular ligand of RAGE. Studies demonstrated that RAGE and Diaph1 act together, and their downstream signaling pathways play a role in neurodegeneration. Here, based on current evidence and our own research, we provide an overview of the RAGE–Diaph1 signaling and discuss the therapeutic potential of targeted therapy aimed at RAGE–Diaph1 signaling inhibition in the prevention and treatment of neurodegenerative diseases.
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spelling doaj-art-1c1935851b5440ddae6cc01490fc7f3f2025-09-26T15:06:41ZengMDPI AGPathophysiology1873-149X2025-08-013234310.3390/pathophysiology32030043Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An OverviewJudyta K. Juranek0Bernard Kordas1Piotr Podlasz2Agnieszka Bossowska3Marta Banach4Department of Human Physiology and Pathophysiology, School of Medicine, University of Warmia and Mazury in Olsztyn, 11-041 Olsztyn, PolandDepartment of Human Physiology and Pathophysiology, School of Medicine, University of Warmia and Mazury in Olsztyn, 11-041 Olsztyn, PolandDepartment of Pathophysiology, Forensic Veterinary Medicine and Administration, Faculty of Veterinary Medicine, University of Warmia and Mazury in Olsztyn, 10-719 Olsztyn, PolandDepartment of Human Physiology and Pathophysiology, School of Medicine, University of Warmia and Mazury in Olsztyn, 11-041 Olsztyn, PolandDepartment of Neurology, Collegium Medicum, Jagiellonian University, 31-530 Kraków, PolandNeurodegenerative diseases are a group of disorders characterized by the progressive deterioration of the structure and function of central nervous system neurons and include, among others, amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), Parkinson’s (PD), Alzheimer’s (AD), and Huntington’s (HD) diseases. And while all these diseases seem to have different genetic and environmental components, growing evidence shows that they share common underlying pathological features such as increased neuroinflammation and excessive oxidative stress. RAGE, the receptor for advanced glycation end-products, is a signal transduction receptor, and its activation triggers an increase in proinflammatory molecules, oxidative stressors, and cytokines. Diaph1, protein diaphanous homolog 1, is an actin modulator and an intracellular ligand of RAGE. Studies demonstrated that RAGE and Diaph1 act together, and their downstream signaling pathways play a role in neurodegeneration. Here, based on current evidence and our own research, we provide an overview of the RAGE–Diaph1 signaling and discuss the therapeutic potential of targeted therapy aimed at RAGE–Diaph1 signaling inhibition in the prevention and treatment of neurodegenerative diseases.https://www.mdpi.com/1873-149X/32/3/43neurodegenerative diseasesreceptor for advanced glycation end-productsDiaph1pathogenesistreatmentsignaling
spellingShingle Judyta K. Juranek
Bernard Kordas
Piotr Podlasz
Agnieszka Bossowska
Marta Banach
Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
neurodegenerative diseases
receptor for advanced glycation end-products
Diaph1
pathogenesis
treatment
signaling
title Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
title_full Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
title_fullStr Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
title_full_unstemmed Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
title_short Current Evidence on the Involvement of RAGE–Diaph1 Signaling in the Pathology and Treatment of Neurodegenerative Diseases—An Overview
title_sort current evidence on the involvement of rage diaph1 signaling in the pathology and treatment of neurodegenerative diseases an overview
topic neurodegenerative diseases
receptor for advanced glycation end-products
Diaph1
pathogenesis
treatment
signaling
url https://www.mdpi.com/1873-149X/32/3/43
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