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Related Concept Videos

Alzheimer Disease ll: Pathophysiology01:23

Alzheimer Disease ll: Pathophysiology

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 microglia. Abnormal...
Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

Huntington disease or HD is a progressive, fatal neurodegenerative disorder inherited in an autosomal dominant pattern.PathophysiologyIt is caused by expansion of the CAG trinucleotide repeat in the HTT gene on chromosome 4 (4p16.3), producing an abnormal huntingtin protein with an expanded polyglutamine tract. This misfolded protein disrupts cellular function, leading to neuronal death. Normal alleles have ≤26 repeats, 27–35 are intermediate (risk of expansion), 36–39 show reduced penetrance,...
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Assumptions of Survival Analysis01:15

Assumptions of Survival Analysis

Survival models analyze the time until one or more events occur, such as death in biological organisms or failure in mechanical systems. These models are widely used across fields like medicine, biology, engineering, and public health to study time-to-event phenomena. To ensure accurate results, survival analysis relies on key assumptions and careful study design.
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

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.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...

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Related Experiment Video

Updated: May 16, 2026

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis
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Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis

Published on: July 16, 2021

[The spread pattern and survival in sporadic ALS].

Fumiharu Kimura1

  • 1Division of Neurology, The First Department of Internal Medicine, Osaka Medical College.

Rinsho Shinkeigaku = Clinical Neurology
|December 1, 2012
PubMed
Summary

The speed of symptom progression in Amyotrophic Lateral Sclerosis (ALS) predicts survival. Rapidly spreading symptoms in ALS patients are linked to shorter survival times.

Area of Science:

  • Neurology
  • Pathology

Context:

  • Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease.
  • A prion-like spread of misfolding pathology is hypothesized in ALS progression.

Purpose:

  • To investigate the pattern and direction of clinical lower motor neuron involvement over time in sporadic ALS patients.
  • To determine the correlation between symptom spread patterns and patient survival.

Summary:

  • This study followed 150 sporadic ALS patients until respiratory symptom onset.
  • The time from symptom onset to the involvement of a second region significantly correlated with survival.
  • A rapid spread pattern (two regions within 3 months) was associated with survival of less than 5 years.
  • Symptom progression in ALS predominantly follows a contiguous, longitudinal pattern, though non-contiguous spread occurred in 13% of cases.

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

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Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis
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Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis

Published on: March 4, 2014

Related Experiment Videos

Last Updated: May 16, 2026

Real-Time Fluorescent Measurement of Synaptic Functions in Models of Amyotrophic Lateral Sclerosis
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Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)
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Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)

Published on: March 17, 2012

Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis
08:16

Utility of Dissociated Intrinsic Hand Muscle Atrophy in the Diagnosis of Amyotrophic Lateral Sclerosis

Published on: March 4, 2014

Impact:

  • Identifies symptom propagation speed as a significant prognostic indicator in ALS.
  • Suggests that understanding the pattern and direction of ALS symptom spread can offer valuable prognostic insights.
  • Supports the concept of a gradual, anatomically directed spread of ALS pathology.