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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,...
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...
Role of Cerebellum and Prefrontal Cortex in Memory01:14

Role of Cerebellum and Prefrontal Cortex in Memory

The cerebellum, while traditionally associated with motor control, also plays a crucial role in memory, particularly in procedural memory, which involves learning motor tasks that become automatic through repetition. For example, studies have shown that when the cerebellum is damaged, individuals or animals lose the ability to learn conditioned motor responses, such as the conditioned eye-blink response in classical conditioning experiments with rabbits. This study demonstrates the cerebellum's...
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'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...
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...

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Related Experiment Video

Updated: May 9, 2026

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
08:43

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment

Published on: August 7, 2017

Prefrontal executive function associated coupling relates to Huntington's disease stage.

Paul G Unschuld1, Xinyang Liu, Megan Shanahan

  • 1Department of Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, USA; Division of Psychiatry Research and Psychogeriatric Medicine, University of Zürich, Zürich, Switzerland.

Cortex; a Journal Devoted to the Study of the Nervous System and Behavior
|August 3, 2013
PubMed
Summary

Huntington's disease (HD) is linked to CAG-repeat expansion in the huntingtin gene. Impaired premotor-medial prefrontal cortex (MPFC) connectivity may indicate early executive dysfunction in prodromal HD.

Keywords:
CognitionCortical networksExecutive functionFunctional connectivityHuntington's diseaseNeurodegenerationfMRI

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A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease
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A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease

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Related Experiment Videos

Last Updated: May 9, 2026

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment
08:43

Application of Granger Causality Analysis of the Directed Functional Connection in Alzheimer's Disease and Mild Cognitive Impairment

Published on: August 7, 2017

A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease
05:39

A Fine Motor Task to Study Joint Kinematics in a Preclinical Model of Neurodegenerative Disease

Published on: June 13, 2025

Area of Science:

  • Neuroscience
  • Genetics
  • Cognitive Science

Background:

  • Huntington's disease (HD) is a neurodegenerative disorder caused by CAG-repeat expansion in the huntingtin (HTT) gene.
  • Executive dysfunction can precede motor symptoms in HD patients.
  • Understanding early functional brain changes is crucial for HD management.

Purpose of the Study:

  • To identify functional network correlates of executive dysfunction in relation to HD stage.
  • To investigate brain connectivity patterns in prodromal and early-stage HD.
  • To explore the relationship between cognitive function, brain networks, and disease progression.

Main Methods:

  • BOLD functional MRI and structural MRI were used in 53 HD mutation carriers (41 prodromal, 12 early affected) and 52 controls.
  • The Tower of London test assessed executive function across varying task complexities during fMRI.
  • Functional brain networks were analyzed based on task-related functional coupling to the medial prefrontal cortex (MPFC).

Main Results:

  • Reduced functional coupling between the premotor cortex and MPFC was observed in prodromal and early manifest HD subjects.
  • Task complexity moderated group differences in connectivity and correlation with HD stage measures.
  • Prodromal HD subjects showed similar performance to controls, yet exhibited altered functional connectivity.

Conclusions:

  • Impaired premotor-MPFC coupling is associated with HD stage-related executive dysfunction.
  • This neural dysfunction may be detectable in prodromal HD subjects before cognitive impairment is clinically apparent.
  • Longitudinal studies are needed to confirm the temporal relationship between impaired connectivity and other HD-related brain changes.