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'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...
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...
Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists01:30

Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists

Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...

You might also read

Related Articles

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

Sort by
Same author

The Right Person, the Right Treatment, at the Right Time in Alzheimer's Disease: Insights From the 2025 Brain Aging Symposium.

Aging cell·2025
Same author

Seeking optimal repeated fluid biomarker assessments to enhance precision and statistical power in clinical trials: SLIM method.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2025
Same author

ω-3 PUFA for Secondary Prevention of White Matter Lesions and Neuronal Integrity Breakdown in Older Adults: A Randomized Clinical Trial.

JAMA network open·2024
Same author

Nutritional metabolism and cerebral bioenergetics in Alzheimer's disease and related dementias.

Alzheimer's & dementia : the journal of the Alzheimer's Association·2022
Same author

Blood plasma protein profiles of neuropsychiatric symptoms and related cognitive decline in older people.

Journal of neurochemistry·2022
Same author

Nutrition state of science and dementia prevention: recommendations of the Nutrition for Dementia Prevention Working Group.

The lancet. Healthy longevity·2022

Related Experiment Video

Updated: May 24, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Ascorbic acid, cognitive function, and Alzheimer's disease: a current review and future direction.

Gene L Bowman1

  • 1Department of Neurology, CR-131, Oregon Health and Science University, Portland, OR, USA. bowmang@ohsu.edu

Biofactors (Oxford, England)
|March 16, 2012
PubMed
Summary

Ascorbic acid (AA), or vitamin C, plays a role in normal brain function and Alzheimer's disease. Further research into AA

More Related Videos

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
08:27

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Related Experiment Videos

Last Updated: May 24, 2026

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells
11:56

A Rapid and Specific Microplate Assay for the Determination of Intra- and Extracellular Ascorbate in Cultured Cells

Published on: April 11, 2014

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein
08:27

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

Published on: July 29, 2018

Area of Science:

  • Neuroscience
  • Nutritional Science
  • Gerontology

Background:

  • Ascorbic acid (AA), a vital nutrient, is investigated for its role in cognitive health.
  • Alzheimer's disease (AD) is a progressive neurodegenerative disorder impacting memory and cognition.
  • Nutritional factors significantly influence brain aging and neurodegenerative disease progression.

Purpose of the Study:

  • To review human and animal studies on ascorbic acid's impact on cognitive function.
  • To explore the relationship between ascorbic acid and Alzheimer's disease.
  • To propose a framework for understanding nutrition's effect on brain aging.

Main Methods:

  • Narrative review of existing scientific literature.
  • Appraisal of human and animal research studies.
  • Synthesis of findings related to ascorbic acid intake, status, metabolism, and brain transport.

Main Results:

  • Evidence suggests ascorbic acid is implicated in normal cognitive processes.
  • The review examines the potential role of ascorbic acid in Alzheimer's disease pathogenesis.
  • A framework is presented to guide future research on nutrition and brain aging.

Conclusions:

  • Ascorbic acid status and metabolism are critical for healthy brain aging.
  • Further investigation is needed to elucidate the precise mechanisms of AA in cognition and AD.
  • Optimizing AA nourishment may offer therapeutic or preventative strategies for cognitive decline.