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: Treatment01:22

Alzheimer's Disease: Treatment

Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
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...
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...
Drugs Affecting Neurotransmitter Synthesis01:29

Drugs Affecting Neurotransmitter Synthesis

Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase, which converts...
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...

You might also read

Related Articles

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

Sort by
Same author

The PDE5 inhibitor vardenafil enhances glutamatergic transmission through amyloid-beta and cellular prion protein.

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics·2026
Same author

Mechanisms Underlying Cancer Chemoresistance: A Starting Point to Identify New Anticancer Strategies.

International journal of molecular sciences·2026
Same author

Quaternary Phosphonium Salts Outperformed Vemurafenib (PLX) and Etoposide Against BRAF<sup>V600D,V600E</sup> PLX-Resistant Melanoma and MDR Neuroblastoma, Exhibiting No/Low Toxicity on 3T3/HaCaT Cells.

International journal of molecular sciences·2026
Same author

Design and Synthesis of New Coumarin Hybrids Active Against Drug-Sensitive and Drug-Resistant Neuroblastoma Cells.

Antioxidants (Basel, Switzerland)·2026
Same author

Impact of anticancer drugs on human Tenon's fibroblast proliferation: implications for glaucoma surgery.

BMJ open ophthalmology·2026
Same author

Prophylactic PDE4 and PDE4B inhibition reduce lesion size and neutrophil infiltration following ischemic stroke in male mice.

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism·2025

Related Experiment Video

Updated: Jul 16, 2026

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans
07:04

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans

Published on: August 15, 2020

Vitamin E and neurodegenerative diseases.

Roberta Ricciarelli1, Francesca Argellati, Maria A Pronzato

  • 1Department of Experimental Medicine, via L.B. Alberti 2, 16132 Genoa, Italy. ricciarelli@medicina.unige.it

Molecular Aspects of Medicine
|February 20, 2007
PubMed
Summary

Vitamin E is crucial for brain health. Its antioxidant properties show promise in potentially preventing and treating neurological disorders like Alzheimer's and Parkinson's disease.

More Related Videos

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

Related Experiment Videos

Last Updated: Jul 16, 2026

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans
07:04

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans

Published on: August 15, 2020

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status
07:08

A High Throughput, Multiplexed and Targeted Proteomic CSF Assay to Quantify Neurodegenerative Biomarkers and Apolipoprotein E Isoforms Status

Published on: October 20, 2016

Area of Science:

  • Neuroscience
  • Biochemistry
  • Antioxidant Research

Background:

  • Vitamin E is vital for neurological function.
  • Oxidative stress is implicated in neurodegenerative diseases.
  • Vitamin E's antioxidant capacity suggests a therapeutic role.

Purpose of the Study:

  • To review the role of vitamin E in neurological disorders.
  • To explore vitamin E's potential in preventing/treating neurodegeneration.

Main Methods:

  • Literature review of existing studies.
  • Analysis of vitamin E's antioxidant mechanisms.
  • Examination of clinical evidence for specific neurological conditions.

Main Results:

  • Vitamin E's essential role in maintaining brain health is confirmed.
  • Evidence links oxidative stress to neurodegeneration.
  • Vitamin E shows potential therapeutic benefits for certain neurological conditions.

Conclusions:

  • Vitamin E's antioxidant properties are significant for neurological health.
  • Further research into vitamin E for Alzheimer's, Parkinson's, ALS, and ataxia is warranted.
  • Vitamin E may offer a preventative or therapeutic strategy against neurodegenerative diseases.