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

35
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...
35
Alzheimer Disease l: Introduction01:29

Alzheimer Disease l: Introduction

21
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...
21
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

1.7K
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...
1.7K
Dementia l: Introduction01:22

Dementia l: Introduction

35
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...
35
Parkinson Disease ll: Pathophysiology01:24

Parkinson Disease ll: Pathophysiology

28
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...
28
Alzheimer's Disease: Treatment01:22

Alzheimer's Disease: Treatment

1.3K
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...
1.3K

You might also read

Related Articles

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

Sort by
Same author

Current and emerging avenues for Alzheimer's disease drug targets.

Journal of internal medicine·2019
Same author

Can LDL cholesterol be too low? Possible risks of extremely low levels.

Journal of internal medicine·2017
Same author

Resistance training does not have an effect on cognition or related serum biomarkers in nonagenarians: a randomized controlled trial.

International journal of sports medicine·2014
Same author

Differences in brain cholesterol metabolism and insulin in two subgroups of patients with different CSF biomarkers but similar white matter lesions suggest different pathogenic mechanisms.

Neuroscience letters·2012
Same author

Ezrin mediates c-Myc actions in prostate cancer cell invasion.

Oncogene·2009
Same author

Involvement of glutaredoxin-1 and thioredoxin-1 in beta-amyloid toxicity and Alzheimer's disease.

Cell death and differentiation·2005
Same journal

Patients with hereditary hemorrhagic telangiectasia have significantly reduced overall survival-And likely by a greater magnitude than we realize.

Journal of internal medicine·2026
Same journal

Social jet lag is associated with incident cardiovascular disease independent of sleep duration and cardiac genetic risk.

Journal of internal medicine·2026
Same journal

Multicenter validation of a severity index model for predicting postoperative acute kidney injury.

Journal of internal medicine·2026
Same journal

The changing epidemiology of human type 2 diabetes-associated atherosclerosis: Pathophysiological mechanisms and emerging treatment possibilities.

Journal of internal medicine·2026
Same journal

Angiopoietin-like protein 3 complete and partial deficiency markedly accelerates apolipoprotein B48 and B100 metabolism in triglyceride-rich lipoproteins in humans.

Journal of internal medicine·2026
Same journal

Authors' reply: Myasthenia gravis following the initiation of statin therapy.

Journal of internal medicine·2026
See all related articles

Related Experiment Video

Updated: May 1, 2026

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

6.6K

Pathways to Alzheimer's disease.

J Hardy, N Bogdanovic, B Winblad

    Journal of Internal Medicine
    |April 22, 2014
    PubMed
    Summary
    This summary is machine-generated.

    Recent Alzheimer's disease trials targeting amyloid failed to show significant clinical benefits. Genetic evidence supports the amyloid hypothesis, suggesting early intervention and targeting genetic variability in amyloid response pathways are key for future Alzheimer's therapies.

    More Related Videos

    Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
    06:23

    Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

    Published on: October 30, 2018

    7.1K
    Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
    09:33

    Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

    Published on: December 26, 2016

    7.6K

    Related Experiment Videos

    Last Updated: May 1, 2026

    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

    6.6K
    Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons
    06:23

    Visualizing Axonal Growth Cone Collapse and Early Amyloid β Effects in Cultured Mouse Neurons

    Published on: October 30, 2018

    7.1K
    Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease
    09:33

    Quantitative 3D In Silico Modeling q3DISM of Cerebral Amyloid-beta Phagocytosis in Rodent Models of Alzheimer's Disease

    Published on: December 26, 2016

    7.6K

    Area of Science:

    • Neuroscience
    • Genetics
    • Pharmacology

    Background:

    • Alzheimer's disease (AD) pathogenesis is strongly linked to amyloid-beta (Aβ) accumulation.
    • Recent clinical trials of anti-amyloid therapies have yielded disappointing or inconclusive results.
    • The precise reasons for the limited efficacy of current anti-amyloid agents remain elusive.

    Purpose of the Study:

    • To investigate the underlying reasons for the lack of clinical success in recent anti-amyloid agent trials for Alzheimer's disease.
    • To evaluate the continued relevance of the amyloid hypothesis in light of new genetic findings.
    • To explore the therapeutic potential of targeting genetic variability in the brain's response to amyloid deposition.

    Main Methods:

    • Review of recent clinical trial data for anti-amyloid agents in Alzheimer's disease.
    • Analysis of recent genetic studies identifying variants in the amyloid gene and related pathways.
    • Integration of genetic findings with the amyloid hypothesis of Alzheimer's disease.

    Main Results:

    • Clinical outcomes from recent anti-amyloid trials in Alzheimer's disease have not demonstrated convincing improvements.
    • Genetic data consistently support the amyloid hypothesis, with identified protective and risk variants.
    • Variability in genetic responses to amyloid deposition suggests potential therapeutic targets.

    Conclusions:

    • The efficacy of anti-amyloid therapies may depend on the stage of Alzheimer's disease, suggesting early intervention is crucial.
    • Genetic variability in amyloid response pathways represents a promising therapeutic avenue for Alzheimer's disease.
    • Further research is warranted to elucidate the complex interplay between genetics, amyloid, and Alzheimer's disease progression.