scholarly journals Absence of HTLV-I and HTLV-II Proviral Genome in the Brains of Patients with Multiple Sclerosis and Amyotrophic Lateral Sclerosis

1992 ◽  
Vol 19 (4) ◽  
pp. 458-461 ◽  
Author(s):  
G.A. Dekaban ◽  
A.J. Hudson ◽  
G.P.A. Rice
Keyword(s):  
Multiple Sclerosis ◽  
Amyotrophic Lateral Sclerosis ◽  
Proviral Genome ◽  
Peripheral Blood Leukocytes ◽  
Serological Evidence ◽  
Blood Leukocytes ◽  
Retroviral Infection ◽  
The Central Nervous System ◽  
Multiple Sclerosis Patients ◽  
Lateral Sclerosis

ABSTRACT:Previous studies have failed to provide serological evidence to incriminate a retroviral infection in the cause of multiple sclerosis. Gene amplification techniques have also failed to identify retroviral footprints in DNA from peripheral blood leukocytes. Here we provide evidence that proviral DNA of HTLV-I and HTLV-II is not found in the central nervous system tissues of patients with multiple sclerosis, patients with amyotrophic lateral sclerosis and controls.

scholarly journals The Expression Discrepancy And Characteristics of Long Non-Coding RNAs In Peripheral Blood Leukocytes From Amyotrophic Lateral Sclerosis Patients

2021 ◽  
Author(s):  
Yujiao Yu ◽  
Dejiang Pang ◽  
Chunyu Li ◽  
Xiaojing Gu ◽  
Yongping Chen ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Transcription Factors ◽  
Peripheral Blood ◽  
Functional Enrichment ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Altered Expression ◽  
Sporadic Als ◽  
Non Coding Rnas ◽  
Lateral Sclerosis

Abstract Amyotrophic lateral sclerosis (ALS) is known to be a progressive neurodegenerative disease that affects upper and lower motor neurons. Less than 10% of ALS patients are defined as familial ALS, more than 90% are sporadic ALS (SALS). According to the genomic information described in existing databases, up to 98% of the human genome consists of non-coding sequences. Nearly 40% of long non-coding RNAs (lncRNAs) are specifically expressed in the brain. We believe that the discrepancy of lncRNAs expression plays a key role in neurodegenerative diseases. We screened 30 lncRNAs with altered expression from peripheral blood leukocytes of SALS patients by microarray and validated 13 of them in leukocytes of SALS, Parkinson's disease (PD) patients and healthy controls (HC). We followed the bioinformatics to perform a functional enrichment analysis of co-expressed mRNAs, transcription factors and lncRNAs for functional prediction. We identified lnc-DYRYK2-7:1, lnc-ABCA12-3:1 and lnc-POTEM-4:7 show decreased expression in SALS patients, whereas in PD patients they show increased expression or no change. In addition, expression of lnc-CNTN4-2:1 and lnc-NR3C2-8:1 were decreased in both SALS and PD patients. We found that XIST was only reduced in male patients with SALS and PD, and not in female patients with SALS but was elevated in PD by gender grouping. We also performed GO term enrichment and KEGG pathway analysis for lncRNAs showing differential expression in microarray. We discovered that a significant proportion of differential expressed lncRNAs were associated with various signaling pathways and transcription factors which are consistent with other clinical findings.

scholarly journals The Expression Discrepancy and Characteristics of Long Non-Coding RNAs in Peripheral Blood Leukocytes From Amyotrophic Lateral Sclerosis Patients

2021 ◽  
Author(s):  
Yujiao Yu ◽  
Dejiang Pang ◽  
Chunyu Li ◽  
Xiaojing Gu ◽  
Yongping Chen ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Transcription Factors ◽  
Neurodegenerative Diseases ◽  
Peripheral Blood ◽  
Functional Enrichment ◽  
Peripheral Blood Leukocytes ◽  
Blood Leukocytes ◽  
Altered Expression ◽  
Non Coding Rnas ◽  
Lateral Sclerosis

Abstract Background Amyotrophic lateral sclerosis (ALS) is known to be a progressive neurodegenerative disease that affects upper and lower motor neurons. Less than 10% of ALS patients are defined as familial ALS, more than 90% are sporadic ALS (SALS). According to the genomic information described in existing databases, up to 98% of the human genome consists of non-coding sequences. And of these, nearly 40% of long non-coding RNAs (lncRNAs) are specifically expressed in the brain. Hence, we believe the discrepancy of lncRNAs expression plays a key role in neurodegenerative diseases. It is demanded to search for potential lncRNA biomarkers of SALS and find their involvement in related disease mechanisms. Methods We screened 30 lncRNAs with altered expression from peripheral blood leukocytes of SALS patients by microarray and validated 13 of them in leukocytes of SALS, Parkinson's disease (PD) patients and healthy controls (HC). The statistical evaluation of expression was performed by the two-tailed Mann-Whitney U test for means between groups. We followed the bioinformatics to perform a functional enrichment analysis of co-expressed mRNAs, transcription factors and lncRNAs for functional prediction. Co-expressed mRNAs of lncRNAs were identified by calculating Pearson Correlation. Results We identified lnc-DYRYK2-7:1, lnc-ABCA12-3:1 and lnc-POTEM-4:7 show decreased expression in SALS patients, whereas in PD patients they show increased expression or no change. In addition, expression of lnc-CNTN4-2:1 and lnc-NR3C2-8:1 were decreased in both SALS and PD patients. We found that XIST was only reduced in male patients with SALS and PD, and not in female patients with SALS but was elevated in PD by gender grouping. Furthermore, we performed GO term enrichment and KEGG pathway analysis for lncRNAs showing differential expression in microarray. We discovered that a significant proportion of differential expressed lncRNAs were associated with various signaling pathways and transcription factors which are consistent with other clinical findings. Conclusion Our study enriches the analysis of lncRNA transcriptome sequencing for ALS and PD to date. We validated 3 lncRNA transcripts with specific expression differences only in SALS patients and investigated the bioinformatics information of lncRNAs for subsequent functional studies related to neurodegenerative diseases.

Cold-induced reactivity in multiple sclerosis patients

2017 ◽  
pp. 56-62 ◽  
Author(s):  
Л.И. Герасимова-Мейгал ◽  
И.М. Сиренев
Keyword(s):  
Multiple Sclerosis ◽  
Cold Test ◽  
Typical Feature ◽  
Humid Climate ◽  
Ssr Analysis ◽  
Epidemiological Surveys ◽  
The Central Nervous System ◽  
The Individual ◽  
Hands And Feet ◽  
Multiple Sclerosis Patients

Цель исследования - изучение особенностей восприимчивости пациентов с рассеянным склерозом (РС) к холодовому воздействию с помощью функциональных тестов, характеризующих функцию терморегуляции. Как известно, РС - хроническое прогрессирующее аутоиммунное заболевание центральной нервной системы мультифакториальной природы, более часто встречающееся в регионах с холодным и влажным климатом. Нарушения терморегуляции вследствие автономной дисфункции являются характерным признаком РС, вместе с тем участию холодового фактора в развитии заболевания не придается существенного значения. Методика. Обследовано 32 пациента (17 мужчин и 15 женщин, средний возраст 29,6 ± 4,2 года) с установленным диагнозом: РС ремиттирующе-рецидивирующая форма течения (средняя продолжительность заболевания - 4,2 ± 2,7 года) и 18 практически здоровых лиц группы сравнения. Восприятие холода оценивали с помощью визуально-аналоговой шкалы. Продолжительность холод-индуцированной вазоконстрикции после локального холодового теста изучали по данным инфракрасной термометрии. Вегетативную регуляцию вазомоторных реакций оценивали по результатам анализа вызванных кожных вегетативных потенциалов (ВКВП). Результаты. На основе анализа самооценки восприятия холода у пациентов с РС показана низкая переносимость холодового фактора. При проведении локального холодового теста отмечено замедление восстановления температуры кожи кисти, что характерно для усиления холод-индуцированной вазоконстрикции. В группе пациентов с РС выявлено снижение параметров ВКВП ладоней и стоп, свидетельствующее о дефиците нейрогенного контроля терморегуляционных сосудистых реакций. Заключение. У пациентов с РС выявлены нарушения механизмов терморегуляции при действии холода, что обусловливает высокую индивидуальную восприимчивость к холоду у данной категории лиц. Сопоставление результатов анализа механизмов индивидуальной холод-индуцированной реактивности у пациентов с РС с данными эпидемиологических исследований приводит к заключению о потенциальном модулирующем влиянии холодового фактора на течение РС. The purpose of the present study was focused on the evaluation of the sensitivity to cold in multiple sclerosis (MS) patients by means of functional thermoregulatory based tests. MS is known to be a chronic autoimmune progressive disease of the central nervous system of multifactor origin that is very common in regions with cold and humid climate. Disorder of thermoregulation caused by autonomic dysfunction is a typical feature of MS, however the role of the cold in the disease development is still underestimated. Methods. Thirty two MS patients (17 males, 15 females, mean age 29,6 ± 4,2 years) with the remittent form of the disease (mean disease duration 4,2 ± 2,7 years) and 18 age-matched healthy controls volunteered to participate in this study. Susceptibility to cold was analyzed with the use of visual-analogous scale. The duration of cold-induced vasoconstriction after local cold test was estimated using by infrared thermometry. Autonomic regulation of vasomotor reactions was investigated with the help of the skin sympathetic response (SSR) analysis. Results. The analysis of self-reported perception of the cold in MS patients showed their low tolerance to cold. Slow recovery of the skin temperature of the hand in the local cold test observed in MS patients was considered as the aggravated cold-induced vasoconstriction. The decreased SSR in the hands and feet in MS patients was found that indicates the deficit of the neurogenic control of thermoregulatory vasomotor reactions. Conclusion. The results obtained demonstrate the impairment of thermoregulation under cold in MS patients that leads to higher individual susceptibility to cold of this group. Comparing of the data found in this study on the mechanisms of the individual cold-induced reactivity in MS patients with epidemiological surveys enable to conclude that cold environment has potential modulating effect of on the course of MS.

scholarly journals Occupational Therapy Interventions in Adults with Multiple Sclerosis or Amyotrophic Lateral Sclerosis: A Scoping Review

2021 ◽  
Vol 18 (4) ◽  
pp. 1432
Author(s):  
Luis De-Bernardi-Ojuel ◽  
Laura Torres-Collado ◽  
Manuela García-de-la-Hera
Keyword(s):  
Multiple Sclerosis ◽  
Amyotrophic Lateral Sclerosis ◽  
Occupational Therapy ◽  
Scoping Review ◽  
Adult Population ◽  
Falls Prevention ◽  
Targeted Interventions ◽  
Therapy Interventions ◽  
Occupational Therapy Interventions ◽  
Lateral Sclerosis

This scoping review aims to describe occupational therapy interventions carried out with multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS) patients in occupational therapy. A peer review of the literature was conducted in different databases: Pubmed, Scopus, Web of Science and Embase, and in some occupational therapy journals. A search of the literature published was carried out before December 2019. The inclusion criteria were as follows: (1) articles evaluating the intervention of occupational therapy in MS or ALS including experimental, randomized, nonrandomized and exploratory studies; (2) written in English or Spanish; (3) adult population (over 18 years old). The initial search identified 836 articles of which we included 32 divided into four areas of intervention: fatigue-targeted interventions, cognitive interventions, physical interventions and others. Only 16 studies were carried out exclusively by occupational therapists. Most occupational therapy interventions are aimed at fatigue and physical rehabilitation. The majority of the studies in our review included MS patients, with little representation from the ALS population. These interventions have shown an improvement in perceived fatigue, manual dexterity, falls prevention and improvement in cognitive aspects such as memory, communication, depression and quality of life in the MS and ALS populations.

scholarly journals The Skeletal Muscle Emerges as a New Disease Target in Amyotrophic Lateral Sclerosis

2021 ◽  
Vol 11 (7) ◽  
pp. 671
Author(s):  
Oihane Pikatza-Menoio ◽  
Amaia Elicegui ◽  
Xabier Bengoetxea ◽  
Neia Naldaiz-Gastesi ◽  
Adolfo López de Munain ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Amyotrophic Lateral Sclerosis ◽  
Muscle Tissue ◽  
Motor Neurons ◽  
Neurodegenerative Disorder ◽  
Disease Onset ◽  
Fine Tuning ◽  
Current State ◽  
The Central Nervous System ◽  
Lateral Sclerosis

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder that leads to progressive degeneration of motor neurons (MNs) and severe muscle atrophy without effective treatment. Most research on ALS has been focused on the study of MNs and supporting cells of the central nervous system. Strikingly, the recent observations of pathological changes in muscle occurring before disease onset and independent from MN degeneration have bolstered the interest for the study of muscle tissue as a potential target for delivery of therapies for ALS. Skeletal muscle has just been described as a tissue with an important secretory function that is toxic to MNs in the context of ALS. Moreover, a fine-tuning balance between biosynthetic and atrophic pathways is necessary to induce myogenesis for muscle tissue repair. Compromising this response due to primary metabolic abnormalities in the muscle could trigger defective muscle regeneration and neuromuscular junction restoration, with deleterious consequences for MNs and thereby hastening the development of ALS. However, it remains puzzling how backward signaling from the muscle could impinge on MN death. This review provides a comprehensive analysis on the current state-of-the-art of the role of the skeletal muscle in ALS, highlighting its contribution to the neurodegeneration in ALS through backward-signaling processes as a newly uncovered mechanism for a peripheral etiopathogenesis of the disease.

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