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Related Concept Videos

Huntington Disease l: Introduction01:21

Huntington Disease l: Introduction

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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...
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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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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...
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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...
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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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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.
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Related Experiment Video

Updated: May 1, 2026

Fractionation for Resolution of Soluble and Insoluble Huntingtin Species
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Huntington's disease.

Chiara Zuccato1, Elena Cattaneo

  • 1Department of Biosciences and Centre for Stem cell Research, Università degli Studi di Milano, Via Viotti 3/5, 20133, Milan, Italy, chiara.zuccato@unimi.it.

Handbook of Experimental Pharmacology
|March 27, 2014
PubMed
Summary
This summary is machine-generated.

Huntington's disease (HD) involves abnormal brain-derived neurotrophic factor (BDNF) due to the huntingtin protein mutation. Lowering BDNF levels in the brain contributes to HD symptoms, with research exploring ways to increase BDNF for treatment.

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Area of Science:

  • Neuroscience
  • Genetics
  • Molecular Biology

Background:

  • Alterations in brain-derived neurotrophic factor (BDNF) are observed in various neurodegenerative disorders.
  • Huntington's disease (HD) is unique, with experiments mechanistically linking genetic defects to BDNF abnormalities.
  • The huntingtin protein, mutated in HD, plays a role in neuronal BDNF regulation.

Purpose of the Study:

  • To elucidate the role of huntingtin protein in the physiological control of BDNF synthesis and transport.
  • To describe how these BDNF processes are disrupted in Huntington's disease.
  • To review preclinical data on manipulating BDNF levels for HD treatment.

Main Methods:

  • Review of molecular mechanisms underlying huntingtin protein's effect on BDNF.
  • Analysis of gain- and loss-of-function experiments in HD models.
  • Discussion of preclinical studies on experimental BDNF level manipulation.

Main Results:

  • Huntingtin protein is integral to neuronal BDNF synthesis and transport.
  • Both BDNF synthesis and transport are disrupted in Huntington's disease.
  • Reduced brain BDNF levels correlate with clinical manifestations of HD.

Conclusions:

  • Loss of brain BDNF contributes significantly to Huntington's disease pathology.
  • Experimental strategies to boost brain BDNF levels show promise for HD treatment.
  • Targeting BDNF represents a potential therapeutic avenue for Huntington's disease.