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Related Concept Videos

Cross-bridge Cycle01:26

Cross-bridge Cycle

As muscle contracts, the overlap between the thin and thick filaments increases, decreasing the length of the sarcomere—the contractile unit of the muscle—using energy in the form of ATP. At the molecular level, this is a cyclic, multistep process that involves binding and hydrolysis of ATP, and movement of actin by myosin.
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The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
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Parkinson's Disease: Overview

Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is to...
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Alterations in Muscle Tone ll

Alterations in muscle tone are common manifestations of neurological disorders and reflect dysfunction within different nervous system regions. Spasticity, paratonia, and dystonia represent distinct forms of hypertonia, each with unique mechanisms, clinical features, and diagnostic importance.CharacteristicsSpasticity happens from upper motor neuron lesions and is characterized by velocity-dependent resistance to passive movement. Clinical features include:Exaggerated deep tendon reflexesClonus...
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Updated: May 19, 2026

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
15:48

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

Published on: July 29, 2007

Amyotrophic lateral sclerosis.

Albert C Ludolph1, Johannes Brettschneider, Jochen H Weishaupt

  • 1Department of Neurology, Ulm University, Oberer Eselsberg 45, 89081 Ulm, Germany. albert.ludolph@rku.de

Current Opinion in Neurology
|August 25, 2012
PubMed
Summary
This summary is machine-generated.

Recent advances in amyotrophic lateral sclerosis (ALS) research reveal genetic links to frontotemporal degeneration (FTD). While therapies lag, new biomarkers and metabolic targets offer future hope for ALS patients.

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Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)
12:35

Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)

Published on: March 17, 2012

Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease.
  • Recent years have seen significant advancements in understanding ALS.
  • The relationship between ALS and frontotemporal degeneration (FTD) is increasingly recognized.

Purpose of the Study:

  • To review recent remarkable advances in the field of ALS.
  • To summarize progress in molecular neuropathology and genetic discoveries.
  • To discuss the current state of interventional therapies and future therapeutic avenues.

Main Methods:

  • Review of recent neuropathological and genetic studies in ALS.
  • Analysis of findings related to gene mutations (TARDBP, FUS, UBQLN2, C9ORF72).
  • Evaluation of outcomes from recent clinical trials for ALS interventions.

Main Results:

  • Discovery of pathogenic mutations in TARDBP, FUS, UBQLN2, and C9ORF72, linking ALS to FTD.
  • Identification of multiple genetic and cell biological factors in ALS causation.
  • Limited progress in interventional therapies, with notable trial failures (lithium, pioglitazone) but potential hope from dexpramipexol.

Conclusions:

  • Significant progress in ALS research driven by neuropathological and genetic discoveries.
  • Metabolism and nutrition are emerging as potential therapeutic targets.
  • Development of standardized biomarkers is crucial for efficient clinical trials in ALS.