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Related Concept Videos

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Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
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Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
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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...
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Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
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Related Experiment Video

Updated: May 3, 2026

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
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Why is ALS so Difficult to Treat?

John Turnbull

    The Canadian Journal of Neurological Sciences. Le Journal Canadien Des Sciences Neurologiques
    |February 19, 2014
    PubMed
    Summary

    Amyotrophic lateral sclerosis (ALS) research faces challenges due to poor understanding of disease causes. Aberrant protein homeostasis offers a new explanation for ALS pathogenesis, suggesting novel therapeutic strategies.

    Area of Science:

    • Neuroscience
    • Molecular Biology
    • Genetics

    Background:

    • Amyotrophic lateral sclerosis (ALS) remains a challenging neurodegenerative disease with limited treatment options.
    • Current understanding of ALS pathogenesis is insufficient, hindering therapeutic development.
    • Existing research often focuses on individual genetic or environmental factors, failing to explain the common disease phenotype.

    Purpose of the Study:

    • To explore novel explanations for the common terminal pathogenesis observed in Amyotrophic Lateral Sclerosis (ALS).
    • To investigate the role of protein homeostasis in the development of ALS.
    • To propose revised therapeutic strategies based on a new understanding of ALS disease mechanisms.

    Main Methods:

    • Review and synthesis of recent findings in ALS research.

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  • Analysis of overlapping etiological considerations.
  • Focus on the concept of protein homeostasis and its implications.

    • Main Results:

    • Inadequate understanding of disease pathogenesis is a primary reason for therapeutic failures in ALS.
    • Aberrant protein homeostasis is emerging as a unifying explanation for the common phenotype and terminal pathogenesis in ALS.
    • This new perspective suggests that while various factors may predispose to ALS, they do not directly cause the disease.

    Conclusions:

    • A deeper understanding of protein homeostasis is crucial for advancing ALS treatment.
    • Current therapeutic approaches for ALS may need significant revision to address the role of protein misfolding and aggregation.
    • New insights into protein homeostasis offer a more optimistic outlook for developing effective ALS therapies.