scholarly journals Progranulin as a therapeutic target in neurodegenerative diseases

2022 ◽  
Author(s):  
Herve Rhinn ◽  
Nadine Tatton ◽  
Stella McCaughey ◽  
Michael Kurnellas ◽  
Arnon Rosenthal
Keyword(s):  
Neurodegenerative Diseases ◽  
Therapeutic Target

scholarly journals Erratum to: Discoidin Domain Receptor 1 is a therapeutic target for neurodegenerative diseases

2021 ◽  
Author(s):  
Alan J Fowler ◽  
Michaeline Hebron ◽  
Kaluvu Balaraman ◽  
Wangke Shi ◽  
Alexander A Missner ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Discoidin Domain Receptor ◽  
Discoidin Domain Receptor 1

scholarly journals Corticotropin releasing factor-binding protein (CRF-BP) as a potential new therapeutic target in Alzheimer’s disease and stress disorders

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Dorien Vandael ◽  
Natalia V. Gounko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Life Stress ◽  
Binding Protein ◽  
Critical Role ◽  
Treatment Strategies ◽  
Corticotropin Releasing Factor ◽  
Stress Disorders

Abstract Alzheimer’s disease is the most common cause of dementia and one of the most complex human neurodegenerative diseases. Numerous studies have demonstrated a critical role of the environment in the pathogenesis and pathophysiology of the disease, where daily life stress plays an important role. A lot of epigenetic studies have led to the conclusion that chronic stress and stress-related disorders play an important part in the onset of neurodegenerative disorders, and an enormous amount of research yielded valuable discoveries but has so far not led to the development of effective treatment strategies for Alzheimer’s disease. Corticotropin-releasing factor (CRF) is one of the major hormones and at the same time a neuropeptide acting in stress response. Deregulation of protein levels of CRF is involved in the pathogenesis of Alzheimer’s disease, but little is known about the precise roles of CRF and its binding protein, CRF-BP, in neurodegenerative diseases. In this review, we summarize the key evidence for and against the involvement of stress-associated modulation of the CRF system in the pathogenesis of Alzheimer’s disease and discuss how recent findings could lead to new potential treatment possibilities in Alzheimer’s disease by using CRF-BP as a therapeutic target.

scholarly journals P38α MAPK Signaling—A Robust Therapeutic Target for Rab5-Mediated Neurodegenerative Disease

2020 ◽  
Vol 21 (15) ◽  
pp. 5485
Author(s):  
Ursula A. Germann ◽  
John J. Alam
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Neurodegenerative Disease ◽  
Therapeutic Target ◽  
Kinase Inhibitors ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Therapeutic Effects ◽  
P38α Kinase

Multifactorial pathologies, involving one or more aggregated protein(s) and neuroinflammation are common in major neurodegenerative diseases, such as Alzheimer’s disease and dementia with Lewy bodies. This complexity of multiple pathogenic drivers is one potential explanation for the lack of success or, at best, the partial therapeutic effects, respectively, with approaches that have targeted one specific driver, e.g., amyloid-beta, in Alzheimer’s disease. Since the endosome-associated protein Rab5 appears to be a convergence point for many, if not all the most prominent pathogenic drivers, it has emerged as a major therapeutic target for neurodegenerative disease. Further, since the alpha isoform of p38 mitogen-activated protein kinase (p38α) is a major regulator of Rab5 activity and its effectors, a biology that is distinct from the classical nuclear targets of p38 signaling, brain-penetrant selective p38α kinase inhibitors provide the opportunity for significant therapeutic advances in neurogenerative disease through normalizing dysregulated Rab5 activity. In this review, we provide a brief summary of the role of Rab5 in the cell and its association with neurodegenerative disease pathogenesis. We then discuss the connection between Rab5 and p38α and summarize the evidence that through modulating Rab5 activity there are therapeutic opportunities in neurodegenerative diseases for p38α kinase inhibitors.

scholarly journals DNA double-strand breaks: a potential therapeutic target for neurodegenerative diseases

2019 ◽  
Vol 27 (4) ◽  
pp. 345-364 ◽  
Author(s):  
Nidheesh Thadathil ◽  
Roderick Hori ◽  
Jianfeng Xiao ◽  
Mohammad Moshahid Khan
Keyword(s):  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Potential Therapeutic Target ◽  
Strand Breaks

scholarly journals Does Irisin Link Physical Exercise with Alzheimer’s Disease?

2018 ◽  
Author(s):  
Dewan Md. Sumsuzzman ◽  
Yunho Jin ◽  
Jeonghyun Choi ◽  
Sang-Rae Lee ◽  
Yonggeun Hong
Keyword(s):  
Skeletal Muscle ◽  
Physical Exercise ◽  
Neurodegenerative Diseases ◽  
Telomere Length ◽  
Neurotrophic Factors ◽  
Therapeutic Target ◽  
Potential Role ◽  
Human Diseases ◽  
Nervous Systems ◽  
Beneficial Effects

Irisin, a skeletal muscle-secreted myokine, produced in response to physical exercise, has protective functions in both the central and the peripheral nervous systems, including the regulation of brain-derived neurotrophic factors and modification of telomere length. Such beneficial effects may inhibit or delay the emergence of neurodegenerative diseases, including Alzheimer’s disease (AD). This review is based on the hypothesis that irisin produced by physical exercise helps control AD progression. Herein, we describe the physiology of irisin and its potential role in delaying or preventing AD. Although current and ongoing studies on irisin show promising results, further research is required to clarify its potential as a meaningful therapeutic target for treating human diseases.

scholarly journals Mitochondrial abnormalities in Parkinson's disease and Alzheimer's disease: can mitochondria be targeted therapeutically?

2018 ◽  
Vol 46 (4) ◽  
pp. 891-909 ◽  
Author(s):  
Ruby Macdonald ◽  
Katy Barnes ◽  
Christopher Hastings ◽  
Heather Mortiboys
Keyword(s):  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Diseases ◽  
Therapeutic Target ◽  
Mitochondrial Dynamics ◽  
Central Mechanism ◽  
Phenotypic Screening ◽  
Mitochondrial Abnormalities

Mitochondrial abnormalities have been identified as a central mechanism in multiple neurodegenerative diseases and, therefore, the mitochondria have been explored as a therapeutic target. This review will focus on the evidence for mitochondrial abnormalities in the two most common neurodegenerative diseases, Parkinson's disease and Alzheimer's disease. In addition, we discuss the main strategies which have been explored in these diseases to target the mitochondria for therapeutic purposes, focusing on mitochondrially targeted antioxidants, peptides, modulators of mitochondrial dynamics and phenotypic screening outcomes.

Sign in / Sign up

Export Citation Format

Share Document