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

Neural Regulation01:37

Neural Regulation

39.6K
Digestion begins with a cephalic phase that prepares the digestive system to receive food. When our brain processes visual or olfactory information about food, it triggers impulses in the cranial nerves innervating the salivary glands and stomach to prepare for food.
39.6K
Alzheimer's Disease: Overview01:26

Alzheimer's Disease: Overview

527
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...
527
Long-term Potentiation01:35

Long-term Potentiation

55.4K
Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre- and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
55.4K
Parkinson's Disease: Overview01:15

Parkinson's Disease: Overview

606
Neurodegenerative disorders are progressive diseases that cause irreversible damage and loss to neurons in specific brain areas. Examples of these disorders include Parkinson's disease, Alzheimer's disease, Multiple Sclerosis (MS), and Amyotrophic Lateral Sclerosis (ALS). These disorders share characteristics such as proteinopathies, selective neuronal vulnerability, and a complex interplay between genetic and environmental factors. The primary therapeutic goal for these conditions is...
606

You might also read

Related Articles

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

Sort by
Same author

Survival estimates and their predictors in genetic frontotemporal dementia: an international, retrospective, cohort study.

The Lancet. Neurology·2026
Same author

Attitudes of specialist memory-clinic patients with early symptomatic Alzheimer's disease towards lecanemab: results from a multicenter survey in Europe.

Scientific reports·2026
Same author

Study protocol: double-blind, randomized, prospective, placebo controlled parallel group phase II study to investigate the effect of glycerol phenylbutyrate (GPB) on neurofilament light chain (NfL) levels in patients with corticobasal syndrome (CBS).

Neurological research and practice·2026
Same author

Head-to-head comparison of neurodegeneration biomarkers across two analytical platforms in Alzheimer's disease.

Aging clinical and experimental research·2026
Same author

[Dementia with Lewy bodies].

Fortschritte der Neurologie-Psychiatrie·2026
Same author

Trajectories of brain structure and function in young adult carriers of genetic frontotemporal dementia variants.

medRxiv : the preprint server for health sciences·2026

Related Experiment Video

Updated: Jul 25, 2025

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry
12:31

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Published on: December 8, 2015

15.1K

Tipping points in neurodegeneration.

Mikael Simons1, Johannes Levin2, Martin Dichgans3

  • 1Institute of Neuronal Cell Biology, Technical University Munich, Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany; Munich Cluster of Systems Neurology (SyNergy), Munich, Germany; Institute for Stroke and Dementia Research, University Hospital of Munich, LMU Munich, Munich, Germany.

Neuron
|June 29, 2023
PubMed
Summary

Alzheimer's disease (AD) pathology develops slowly. Resilience factors in the glial, immune, and vascular systems are crucial in preventing dementia transition, offering new therapeutic targets.

Keywords:
Alzheimer's diseasegliainflammationneurodegenerationvasculature

More Related Videos

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

17.3K
Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae
07:14

Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae

Published on: February 25, 2022

6.0K

Related Experiment Videos

Last Updated: Jul 25, 2025

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry
12:31

Sensitive Detection of Proteopathic Seeding Activity with FRET Flow Cytometry

Published on: December 8, 2015

15.1K
Evaluation of Synapse Density in Hippocampal Rodent Brain Slices
07:44

Evaluation of Synapse Density in Hippocampal Rodent Brain Slices

Published on: October 6, 2017

17.3K
Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae
07:14

Optogenetic Phase Transition of TDP-43 in Spinal Motor Neurons of Zebrafish Larvae

Published on: February 25, 2022

6.0K

Area of Science:

  • Neuroscience
  • Pathology
  • Immunology

Background:

  • Alzheimer's disease (AD) is characterized by slow amyloid-beta (Aβ) plaque formation preceding neurodegeneration and dementia.
  • A significant number of individuals with AD pathology do not develop dementia, indicating the presence of protective factors.

Purpose of the Study:

  • To explore resilience and resistance factors beyond cognitive reserve in Alzheimer's disease.
  • To propose a framework focusing on 'tipping points' and non-neuronal mechanisms in preclinical AD.

Main Methods:

  • Review of existing evidence on resilience and resistance factors in AD.
  • Application of the 'tipping points' metaphor to explain the transition from preclinical AD to dementia.

Main Results:

  • Resilience is influenced by glial, immune, and vascular systems, extending beyond cognitive reserve.
  • Loss of adaptive functions in these systems, coupled with AD pathology, can trigger dementia.

Conclusions:

  • Non-neuronal systems play a critical role in AD resilience.
  • Targeting these resilience mechanisms and understanding tipping points may offer novel therapeutic strategies for preclinical AD.