scholarly journals An Overview of Potential Targets for Treating Amyotrophic Lateral Sclerosis and Huntington’s Disease

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Caroline Zocatelli de Paula ◽  
Bruno Daniel Correia Gonçalves ◽  
Luciene Bruno Vieira
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Neurodegenerative Diseases ◽  
Physical Health ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Scientific Community ◽  
Progressive Damage ◽  
Mental And Physical Health ◽  
Lateral Sclerosis

Neurodegenerative diseases affect millions of people worldwide. Progressive damage or loss of neurons, neurodegeneration, has severe consequences on the mental and physical health of a patient. Despite all efforts by scientific community, there is currently no cure or manner to slow degeneration progression. We review some treatments that attempt to prevent the progress of some of major neurodegenerative diseases: Amyotrophic Lateral Sclerosis and Huntington’s disease.

scholarly journals A modular tool to query and inducibly disrupt biomolecular condensates

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Carmen N. Hernández-Candia ◽  
Sarah Pearce ◽  
Chandra L. Tucker
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Cellular Function ◽  
Biological Role ◽  
Cellular Biology ◽  
Condensate Formation ◽  
Health And Disease ◽  
Lateral Sclerosis

AbstractDynamic membraneless compartments formed by protein condensates have multifunctional roles in cellular biology. Tools that inducibly trigger condensate formation have been useful for exploring their cellular function, however, there are few tools that provide inducible control over condensate disruption. To address this need we developed DisCo (Disassembly of Condensates), which relies on the use of chemical dimerizers to inducibly recruit a ligand to the condensate-forming protein, triggering condensate dissociation. We demonstrate use of DisCo to disrupt condensates of FUS, associated with amyotrophic lateral sclerosis, and to prevent formation of polyglutamine-containing huntingtin condensates, associated with Huntington’s disease. In addition, we combined DisCo with a tool to induce condensates with light, CRY2olig, achieving bidirectional control of condensate formation and disassembly using orthogonal inputs of light and rapamycin. Our results demonstrate a method to manipulate condensate states that will have broad utility, enabling better understanding of the biological role of condensates in health and disease.

Acoustic Analysis of Voices of Patients with Neurologic Disease: Rationale and Preliminary Data

1988 ◽  
Vol 97 (2) ◽  
pp. 164-172 ◽  
Author(s):  
Lorraine A. Ramig ◽  
Ingo R. Titze ◽  
Ronald C. Scherer ◽  
Steven P. Ringel
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Preliminary Data ◽  
Acoustic Analysis ◽  
Neurologic Disease ◽  
Clinical Value ◽  
Neurologic Disorders ◽  
Speech Pathologist ◽  
Lateral Sclerosis

This paper presents a rationale for acoustic analysis of voices of neurologically diseased patients, and reports preliminary data from patients with myotonic dystrophy, Huntington's disease, Parkinson's disease, and amyotrophic lateral sclerosis, as well as from individuals at risk for Huntington's disease. Noninvasive acoustic analysis may be of clinical value to the otolaryngologist, neurologist, and speech pathologist for early and differential diagnosis and for documenting disease progression in these various neurologic disorders.

Huntington's disease presenting as amyotrophic lateral sclerosis

2009 ◽  
pp. 1-3 ◽  
Author(s):  
Julie Phukan ◽  
Elfatih Ali ◽  
Niall Pender ◽  
Fiona Molloy ◽  
Michael Hennessy ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Lateral Sclerosis

Prevalence of Huntington's disease gene CAG repeat alleles in sporadic amyotrophic lateral sclerosis patients

2012 ◽  
Vol 13 (3) ◽  
pp. 265-269 ◽  
Author(s):  
Eliana Marisa Ramos ◽  
Pamela Keagle ◽  
Tammy Gillis ◽  
Patrick Lowe ◽  
Jayalakshmi S. Mysore ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Disease Gene ◽  
Cag Repeat ◽  
Sporadic Amyotrophic Lateral Sclerosis ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis and Huntington’s disease: Neurodegenerative link or coincidence?

2013 ◽  
Vol 15 (1-2) ◽  
pp. 145-147 ◽  
Author(s):  
Suresh Kumar Chhetri ◽  
Rejith Dayanandan ◽  
Dorothea Bindman ◽  
David Craufurd ◽  
Tahir Majeed
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Huntington's Disease ◽  
Huntington’S Disease ◽  
Lateral Sclerosis

scholarly journals Common Factors in Neurodegeneration: A Meta-Study Revealing Shared Patterns on a Multi-Omics Scale

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2642
Author(s):  
Nicolas Ruffini ◽  
Susanne Klingenberg ◽  
Susann Schweiger ◽  
Susanne Gerber
Keyword(s):  
Immune Response ◽  
Amyotrophic Lateral Sclerosis ◽  
Neurodegenerative Diseases ◽  
Huntington's Disease ◽  
Humoral Immune Response ◽  
Differentially Expressed ◽  
Humoral Immune ◽  
Proteomic Data ◽  
Go Terms ◽  
Lateral Sclerosis

Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) are heterogeneous, progressive diseases with frequently overlapping symptoms characterized by a loss of neurons. Studies have suggested relations between neurodegenerative diseases for many years (e.g., regarding the aggregation of toxic proteins or triggering endogenous cell death pathways). We gathered publicly available genomic, transcriptomic, and proteomic data from 177 studies and more than one million patients to detect shared genetic patterns between the neurodegenerative diseases on three analyzed omics-layers. The results show a remarkably high number of shared differentially expressed genes between the transcriptomic and proteomic levels for all conditions, while showing a significant relation between genomic and proteomic data between AD and PD and AD and ALS. We identified a set of 139 genes being differentially expressed in several transcriptomic experiments of all four diseases. These 139 genes showed overrepresented gene ontology (GO) Terms involved in the development of neurodegeneration, such as response to heat and hypoxia, positive regulation of cytokines and angiogenesis, and RNA catabolic process. Furthermore, the four analyzed neurodegenerative diseases (NDDs) were clustered by their mean direction of regulation throughout all transcriptomic studies for this set of 139 genes, with the closest relation regarding this common gene set seen between AD and HD. GO-Term and pathway analysis of the proteomic overlap led to biological processes (BPs), related to protein folding and humoral immune response. Taken together, we could confirm the existence of many relations between Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis on transcriptomic and proteomic levels by analyzing the pathways and GO-Terms arising in these intersections. The significance of the connection and the striking relation of the results to processes leading to neurodegeneration between the transcriptomic and proteomic data for all four analyzed neurodegenerative diseases showed that exploring many studies simultaneously, including multiple omics-layers of different neurodegenerative diseases simultaneously, holds new relevant insights that do not emerge from analyzing these data separately. Furthermore, the results shed light on processes like the humoral immune response that have previously been described only for certain diseases. Our data therefore suggest human patients with neurodegenerative diseases should be addressed as complex biological systems by integrating multiple underlying data sources.

Mitochondria and Neurodegeneration

2007 ◽  
Vol 27 (1-3) ◽  
pp. 87-104 ◽  
Author(s):  
Lucia Petrozzi ◽  
Giulia Ricci ◽  
Noemi J. Giglioli ◽  
Gabriele Siciliano ◽  
Michelangelo Mancuso
Keyword(s):  
Alzheimer’S Disease ◽  
Amyotrophic Lateral Sclerosis ◽  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Huntington's Disease ◽  
Neurodegenerative Disorders ◽  
Molecular Abnormalities ◽  
Lateral Sclerosis ◽  
Lines Of Evidence

Many lines of evidence suggest that mitochondria have a central role in ageing-related neurodegenerative diseases. However, despite the evidence of morphological, biochemical and molecular abnormalities in mitochondria in various tissues of patients with neurodegenerative disorders, the question “is mitochondrial dysfunction a necessary step in neurodegeneration?” is still unanswered. In this review, we highlight some of the major neurodegenerative disorders (Alzheimer's disease, Parkinson's disease, Amyotrophic lateral sclerosis and Huntington's disease) and discuss the role of the mitochondria in the pathogenetic cascade leading to neurodegeneration.

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