Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Long-term Depression01:03

Long-term Depression

Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Phase-targeted auditory stimulation enhances slow-wave activity during sleep in Huntington's disease: A pilot crossover study.

Journal of Huntington's disease·2026
Same author

Sodium channel blockers are associated with reduced dementia risk in late-onset unexplained epilepsy.

medRxiv : the preprint server for health sciences·2026
Same author

Outcome associations of CSF total tau in suspected non-Alzheimer pathophysiology.

Journal of neurology·2026
Same author

Health and quality of life in patients with leg lymphedema during maintenance phase.

VASA. Zeitschrift fur Gefasskrankheiten·2026
Same author

[Amyotrophic lateral sclerosis (ALS): current perspectives and the Swiss ALS Registry].

Praxis·2026
Same author

ESTREL-Fatigue-association of levodopa with post-stroke fatigue.

European stroke journal·2026

Related Experiment Video

Updated: Jun 20, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Adaptive metabolic changes in CADASIL white matter.

Tamar Akhvlediani1, Anke Henning, Peter S Sándor

  • 1Department of Neurology, University Hospital Zürich, Frauenklinikstrasse 26, 8091, Zurich, Switzerland.

Journal of Neurology
|August 20, 2009
PubMed
Summary
This summary is machine-generated.

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) shows metabolic changes in white matter. These changes suggest axonal loss and glial cell changes, possibly adapting to reduced blood flow.

More Related Videos

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function
11:47

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

Published on: January 22, 2017

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
09:33

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

Published on: July 28, 2013

Related Experiment Videos

Last Updated: Jun 20, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
09:41

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function
11:47

Treating SCA1 Mice with Water-Soluble Compounds to Non-Specifically Boost Mitochondrial Function

Published on: January 22, 2017

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases
09:33

Diffusion Tensor Magnetic Resonance Imaging in the Analysis of Neurodegenerative Diseases

Published on: July 28, 2013

Area of Science:

  • Neuroimaging
  • Metabolic studies
  • Genetics

Background:

  • Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a genetic cause of stroke.
  • Pathogenic mechanisms and functional alterations in CADASIL are not well understood.

Purpose of the Study:

  • Investigate adaptive metabolic and functional changes in white matter hyperintensities (WMH) and normal-appearing white matter (NAWM) in CADASIL patients.
  • Utilize (1)H-magnetic resonance spectroscopic imaging (MRSI) for detailed metabolic analysis.

Main Methods:

  • Studied eight CADASIL patients and eight matched healthy controls.
  • Acquired (1)H-MRSI data using high-resolution multi-spin echo (T(E) = 288 ms) and medium-resolution MRSI (T(E) = 35 ms) on a 3T scanner.
  • Analyzed metabolic ratios including Cre/Cho, Glx/Cho, Glx/Cre, and mI/Cho.

Main Results:

  • CADASIL patients exhibited characteristic WMH.
  • Significantly decreased Cre/Cho, Glx/Cho, and Glx/Cre ratios in WMH compared to NAWM within patients.
  • Significantly increased Glx/Cre and mI/Cho ratios in NAWM of CADASIL patients compared to controls.
  • Severely affected patients showed decreased NAA concentrations in WMH.

Conclusions:

  • Metabolic abnormalities in WMH are consistent with axonal loss from chronic micro-infarctions.
  • Increased Glx/Cre and mI/Cho in NAWM suggest increased glial cell density and decreased neuronal density.
  • These alterations may represent adaptive responses to hypoperfusion and impaired vasoreactivity in CADASIL NAWM.