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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,...
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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...
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...
Lysosomal Hydrolases01:22

Lysosomal Hydrolases

Lysosomes are the site for the degradation of macromolecules and biological polymers released during membrane trafficking events such as secretory, endocytic, autophagic, and phagocytic pathways. The membrane-enclosed area of the lysosome, called the lumen, contains hydrolytic enzymes active in an acidic environment. These acid hydrolases are functional at a pH between 4.5 and 5 and are involved in cellular processes such as cell signaling, energy metabolism, restoration of the plasma membrane,...
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...
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.
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Updated: Jul 18, 2026

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

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Published on: February 27, 2018

Disgust and Huntington's disease.

Catherine J Hayes1, Richard J Stevenson, Max Coltheart

  • 1Macquarie Centre for Cognitive Science, Macquarie University, Sydney, New South Wales, Australia. psyhcj@nus.edu.sg

Neuropsychologia
|November 28, 2006
PubMed
Summary

Patients with Huntington's disease (HD) show broad difficulties processing disgust, not just facial expressions. This suggests a fundamental deficit in disgust processing across multiple sensory and cognitive domains in HD.

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Area of Science:

  • Neuroscience
  • Psychology
  • Emotion Recognition

Background:

  • Huntington's disease (HD) patients exhibit impaired recognition of facial disgust.
  • This contrasts with amygdala patients' impaired fear recognition, suggesting emotion-specific neural substrates.
  • The study investigates if HD disgust impairment is limited to facial perception or broader.

Purpose of the Study:

  • To determine the scope of disgust processing deficits in Huntington's disease.
  • To investigate whether impairments extend beyond facial perception to other sensory and cognitive domains.
  • To explore the neural basis of emotion processing in neurodegenerative diseases.

Main Methods:

  • Fourteen Huntington's disease patients and 14 healthy controls participated.
  • Evaluated emotion processing across seven tasks: situational knowledge, vocal, lexical, scene, questionnaire, olfactory, and gustatory perception.
  • Assessed verbal and non-verbal aspects of disgust processing.

Main Results:

  • Huntington's disease patients showed preserved verbal disgust processing.
  • Impairments were observed in olfactory disgust, vocal disgust expressions, classifying disgusting pictures, and declarative knowledge of disgust elicitors.
  • These parallel impairments occurred across different input domains.

Conclusions:

  • The findings suggest a fundamental deficit in disgust processing in Huntington's disease.
  • The impairment is not restricted to facial perception but affects multiple modalities.
  • This highlights the complexity of emotion processing deficits in neurodegenerative conditions.