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

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.
siRNA - Small Interfering RNAs02:30

siRNA - Small Interfering RNAs

Small interfering RNAs, or siRNAs, are short regulatory RNA molecules that can silence genes post-transcriptionally, as well as the transcriptional level in some cases. siRNAs are important for protecting cells against viral infections and silencing transposable genetic elements.
In the cytoplasm, siRNA is processed from a double-stranded RNA, which comes from either endogenous DNA transcription or exogenous sources like a virus. This double-stranded RNA is then cleaved by the ATP-dependent...
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 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...

You might also read

Related Articles

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

Sort by
Same author

Experimenting with disembodied human brain might better approximate ground truth but could lack statistical assurance.

Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology·2026
Same author

Linking primary cilia defects to the "Big 3" neurodegenerative diseases - causal, consequential, or correlative?

EXCLI journal·2026
Same author

Possible misplaced perception of moral shame in AI-use disclosure.

Accountability in research·2026
Same author

Letter to the Editor: Citations of Retracted Publications Should Be Discounted From One's Bibliometric Indicator.

Journal of Korean medical science·2026
Same author

Exposure and impact: highlights from the second scientific conference and recent activities of the International Society of Radiation Epidemiology and Dosimetry (ISoRED).

Journal of radiological protection : official journal of the Society for Radiological Protection·2026
Same author

Primary cilium and TULP3-dependent ciliary targeting of ACE2 in SARS-CoV-2 tropism.

Cell communication and signaling : CCS·2025

Related Experiment Video

Updated: Jul 16, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

SIRT1 and neuronal diseases.

Bor Luen Tang1, Christelle En Lin Chua

  • 1Department of Biochemistry, Yong Loo Lin School of Medicine, National University of Singapore, 8 Medical Drive, Singapore 117597, Singapore. bchtbl@nus.edu.sg

Molecular Aspects of Medicine
|April 3, 2007
PubMed
Summary

SIRT1 (silent information regulator 2) protein deacetylase activity shows neuroprotective effects against neurodegenerative diseases like Alzheimer's. Its induction may offer novel therapeutic strategies by reducing neuronal damage and promoting cell survival.

Related Experiment Videos

Last Updated: Jul 16, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
14:32

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • SIRT1 is a protein deacetylase linked to lifespan extension.
  • SIRT1 induction shows promise in mitigating neurodegeneration in Alzheimer's and Huntington's disease models.
  • Neuroprotection by SIRT1 can be achieved through activators like resveratrol or caloric restriction (CR).

Purpose of the Study:

  • To explore the neuroprotective mechanisms of SIRT1.
  • To understand how SIRT1 induction impacts neurodegenerative disease pathways.
  • To identify potential therapeutic targets for neurodegenerative diseases.

Main Methods:

  • Investigated SIRT1's role in non-amyloidogenic amyloid precursor protein cleavage.
  • Examined SIRT1's effect on amyloid beta-peptide clearance.
  • Assessed SIRT1's influence on neuroinflammatory signaling pathways.
  • Analyzed SIRT1's impact on neuronal transcription profiles and anti-apoptotic gene activity.
  • Explored SIRT1's role in Wallerian degeneration slow (Wld(s)) phenotype.

Main Results:

  • SIRT1 induction promotes non-amyloidogenic amyloid precursor protein processing.
  • SIRT1 enhances the clearance of amyloid beta-peptides.
  • SIRT1 may inhibit neuroinflammatory pathways, reducing neuronal damage.
  • Increased SIRT1 activity alters gene expression to boost anti-stress and anti-apoptotic responses.
  • SIRT1 activity is implicated in preventing axonal degeneration.

Conclusions:

  • SIRT1 exhibits significant neuroprotective capabilities through multiple mechanisms.
  • Targeting SIRT1 offers a promising therapeutic avenue for neurodegenerative diseases.
  • Understanding SIRT1's function is crucial for developing novel clinical interventions for aging-related neuronal degeneration.