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Related Concept Videos

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,...
Parkinson's Disease: Overview01:15

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...
Parkinson Disease l: Introduction01:24

Parkinson Disease l: Introduction

Parkinson’s disease is a chronic, progressive neurodegenerative disorder that primarily affects movement. It is characterized by motor symptoms such as resting tremors, muscle rigidity, bradykinesia (slowness of movement), and postural instability. Patients may notice hand tremors at rest, stiffness during movement, or a shuffling gait. In addition to motor features, non-motor symptoms include sleep disturbances, mood and behavioral changes, constipation, and cognitive impairment, all of which...
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

Parkinson disease (PD) is a progressive neurodegenerative disorder primarily affecting movement, with additional non-motor features. Its pathophysiology involves complex interactions among genetic susceptibility, environmental exposures, and cellular dysfunction, including dopaminergic neuron loss, protein aggregation, and mitochondrial impairment.Selective NeurodegenerationA key feature is the degeneration of dopaminergic neurons in the substantia nigra pars compacta, leading to reduced...
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...
Disorders of the Nervous Tissue01:28

Disorders of the Nervous Tissue

Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises from the...

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Related Experiment Video

Updated: May 20, 2026

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
07:08

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Published on: February 27, 2018

Huntington's disease.

Ainhi D Ha1, Victor S C Fung

  • 1Movement Disorders Unit, Department of Neurology, Westmead Hospital, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia.

Current Opinion in Neurology
|July 10, 2012
PubMed
Summary
This summary is machine-generated.

Early detection of Huntington's disease (HD) is possible years before symptoms appear. Research into prodromal HD and its mechanisms offers new therapeutic targets for neuroprotection.

More Related Videos

Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System
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Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System

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Whole-brain Segmentation and Change-point Analysis of Anatomical Brain MRI—Application in Premanifest Huntington's Disease
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Whole-brain Segmentation and Change-point Analysis of Anatomical Brain MRI—Application in Premanifest Huntington's Disease

Published on: June 9, 2018

Related Experiment Videos

Last Updated: May 20, 2026

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
07:08

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species

Published on: February 27, 2018

Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System
10:52

Efficient and Scalable Production of Full-length Human Huntingtin Variants in Mammalian Cells using a Transient Expression System

Published on: December 10, 2021

Whole-brain Segmentation and Change-point Analysis of Anatomical Brain MRI—Application in Premanifest Huntington's Disease
09:06

Whole-brain Segmentation and Change-point Analysis of Anatomical Brain MRI—Application in Premanifest Huntington's Disease

Published on: June 9, 2018

Area of Science:

  • Neuroscience
  • Genetics
  • Clinical Neurology

Background:

  • Huntington's disease (HD) is a progressive neurodegenerative disorder.
  • Early identification of individuals at risk is crucial for timely intervention.
  • Understanding the preclinical stages of HD is key to developing effective treatments.

Purpose of the Study:

  • To review recent advancements in the clinical characterization of prodromal Huntington's disease.
  • To explore the pathophysiological mechanisms underlying HD.
  • To identify potential therapeutic targets for HD treatment.

Main Methods:

  • Review of current literature on prodromal Huntington's disease.
  • Analysis of clinical and neuroradiological findings in pre-symptomatic individuals.
  • Examination of molecular pathways implicated in HD neurodegeneration.

Main Results:

  • Clinical and neuroradiological abnormalities are detectable up to 15 years before overt HD symptoms.
  • Potential biomarkers for disease progression show promise but require further validation.
  • Several molecular pathways involved in neurodegeneration offer targets for therapeutic intervention.

Conclusions:

  • The prodromal stage of HD is an opportune window for disease-modifying therapies.
  • Development of reliable biomarkers for monitoring disease progression is essential for clinical trials.
  • Continued research, particularly using cellular and animal models, is advancing the understanding of HD pathophysiology.