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 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 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'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...
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...
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...
Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders01:27

Psychosis: Pathophysiology of Schizophrenia and Other Psychotic Disorders

Schizophrenia is a neurodevelopmental disorder whose origins are rooted in complex genetic components. Despite our burgeoning understanding, the pathophysiology of this disorder remains incompletely deciphered.
Researchers have identified genetic factors that increase susceptibility to schizophrenia, underscoring the intricate interplay between genetics and environment in disease development. At the core of schizophrenia's pathophysiology is excessive dopaminergic neurotransmission within the...

You might also read

Related Articles

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

Sort by
Same author

Operational Definition of Active and Healthy Ageing (AHA): A Conceptual Framework.

The journal of nutrition, health & aging·2015
Same author

Antioxidant supplements: Effects on disease and aging in the United States population.

Journal of the American Aging Association·2013
Same author

Myctolaimellus robiniae n. sp. (Diplogasterida: Cylindrocorporidae) from Larval Cavities of the Locust Borer, Megacyllene robiniae Forster.

Journal of nematology·2009
Same author

Aging: overview.

Annals of the New York Academy of Sciences·2002
Same author

Development of muscarinic analgesics derived from epibatidine: role of the M4 receptor subtype.

The Journal of pharmacology and experimental therapeutics·1999
Same author

Aging: phenomena and theories.

Annals of the New York Academy of Sciences·1999

Related Experiment Video

Updated: May 12, 2026

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Alzheimer's disease: A hypothesis on pathogenesis.

D Harman1

  • 1Department of Medicine, University of Nebraska College of Medicine, Omaha, NE 68198-4635.

Journal of the American Aging Association
|April 23, 2013
PubMed
Summary

Alzheimer's disease (AD) may stem from accelerated neuronal aging. Genetic mutations in familial AD (FAD) and DNA damage in sporadic AD (SAD) can increase oxidative stress, contributing to AD pathogenesis.

Area of Science:

  • Neuroscience
  • Genetics
  • Aging Research

Background:

  • Alzheimer's disease (AD) is the primary cause of dementia, characterized by brain lesions like plaques and tangles.
  • AD presents as early-onset familial (FAD) or late-onset sporadic (SAD), with FAD linked to specific gene mutations.

Purpose of the Study:

  • To explore a unifying hypothesis for AD pathogenesis, linking both FAD and SAD to accelerated neuronal aging.
  • To investigate the role of endoplasmic reticulum (ER) calcium dysregulation and mitochondrial oxidative stress in AD.

Main Methods:

  • Review of existing literature on AD genetics, molecular mechanisms, and neuropathology.
  • Analysis of the proposed link between genetic mutations (APP, PS1, PS2) and ER calcium homeostasis.
  • Examination of the role of mitochondrial function and oxidative stress in neuronal aging and AD.

More Related Videos

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

Related Experiment Videos

Last Updated: May 12, 2026

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease
06:52

Fabrication of Amyloid-β-Secreting Alginate Microbeads for Use in Modelling Alzheimer's Disease

Published on: July 6, 2019

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
06:02

Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model

Published on: July 26, 2011

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices
07:57

An Alternative Approach to Study Primary Events in Neurodegeneration Using Ex Vivo Rat Brain Slices

Published on: April 11, 2018

Main Results:

  • Mutations in FAD genes (APP, PS1, PS2) may disrupt ER calcium buffering, leading to mitochondrial dysfunction.
  • Mitochondrial calcium overload enhances superoxide radical formation, accelerating neuronal aging.
  • SAD may arise from early-life DNA mutations that promote mitochondrial oxidative stress.

Conclusions:

  • Accelerated neuronal aging, driven by genetic or DNA damage-induced oxidative stress, offers a plausible explanation for both FAD and SAD.
  • Understanding these pathways suggests potential preventative and therapeutic strategies for Alzheimer's disease.