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 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...
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

Identification of XZ8078 as a Dual-Target Degrader Targeting PARP1 and IKZF3 for Broad Spectrum Anticancer Treatment.

Journal of medicinal chemistry·2026
Same author

Genome-wide identification and characterization of the phytochrome family in Gossypium: GhPHYB1 as a dual regulator of plant architecture and drought tolerance in upland cotton.

Plant physiology and biochemistry : PPB·2026
Same author

Health care utilization in veterans with Alzheimer disease.

The American journal of managed care·2026
Same author

Identification and characterization of intracerebral hemorrhage events in elderly veterans with alzheimer's disease in the veterans affairs healthcare system.

Scientific reports·2026
Same author

Bioelectric signals promote diabetic bone regeneration through Piezo1-mediated activation of the efferocytic immune microenvironment.

Bioactive materials·2026
Same author

HOPX is required for the generation of umbilical cord blood-derived memory-like NK cells induced by three cytokines.

Frontiers in immunology·2026
Same journal

Evidence-Based Clinical Recommendations for the Appropriate Use of Diagnostic Tests in Pediatric Allergology: Focus on Asthma, Rhinoconjunctivitis, and Keratoconjunctivitis Vernal.

Journal of clinical medicine·2026
Same journal

Surgical and Transcatheter Approach of a Failed Mitral Valve Repair: A Comprehensive Review on Selecting the Most Suitable Approach.

Journal of clinical medicine·2026
Same journal

Hybrid Metaheuristic Feature Selection for Breast Cancer Detection in Digital Mammography: A Feasibility Study with Nested Validation, Benchmarking, and External Stress Testing.

Journal of clinical medicine·2026
Same journal

Identity Transformation and the Role of Accountability in Recovery from Problematic Pornography Use: A Phenomenological-Hermeneutical Study.

Journal of clinical medicine·2026
Same journal

Does Early Surgical Treatment in Degenerative Cervical Myelopathy Have a Favorable Clinical Outcome and Impact on Quality of Life?

Journal of clinical medicine·2026
Same journal

Shear Wave Elastography in Musculoskeletal Imaging: A Narrative Review.

Journal of clinical medicine·2026
See all related articles

Related Experiment Video

Updated: May 14, 2026

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

Re-Purposing a Rho-Associated Coiled-Coil Kinase (ROCK) Inhibitor for Alzheimer's Disease.

Xavier Cambi1,2, Zhiqing Liu2, Kevin Guo3

  • 1Department of Pharmacology, Physiology and Biophysics, Chobanian & Avedisian School of Medicine, Boston University, Boston, MA 02118, USA.

Journal of Clinical Medicine
|May 13, 2026
PubMed
Summary
This summary is machine-generated.

Netarsudil, an FDA-approved drug, shows potential for Alzheimer's disease (AD) treatment by reducing pathological tau proteins in the brain. This ROCK inhibitor may offer a new therapeutic avenue for AD by demonstrating neuroprotective effects in mice.

Keywords:
AlzheimerROCKefficacypharmacokineticsproteomics

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 14, 2026

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke
09:45

Motor and Hippocampal Dependent Spatial Learning and Reference Memory Assessment in a Transgenic Rat Model of Alzheimer's Disease with Stroke

Published on: March 22, 2016

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
  • Pharmacology
  • Biochemistry

Background:

  • Current Alzheimer's disease (AD) treatments offer limited efficacy or severe side effects.
  • There is a critical need for novel, disease-modifying AD therapeutics.

Purpose of the Study:

  • To investigate the potential of netarsudil, a Rho-associated kinase (ROCK) inhibitor, as a novel therapeutic agent for Alzheimer's disease (AD).
  • To evaluate netarsudil's ability to reduce pathological tau proteins and its neuroprotective effects in vivo.

Main Methods:

  • Pharmacokinetic and pharmacodynamic studies of netarsudil in wild-type mice following intraperitoneal injection.
  • Quantification of tau and phosphorylated tau (ptau) using ELISA.
  • Proteomic analysis of mouse brains to identify molecular changes.

Main Results:

  • Netarsudil demonstrated brain permeability with sustained central nervous system (CNS) exposure.
  • A significant negative correlation was observed between netarsudil levels and brain tau/ptau.
  • Proteomic analysis revealed altered mitochondrial function and modulation of specific genes (Mt1, Mt2, Pzp, Serpina3m).

Conclusions:

  • Netarsudil effectively reduces AD pathological markers (tau/ptau) in a preclinical model.
  • The observed neuroprotective proteomic profile supports netarsudil's potential as a novel therapeutic for Alzheimer's disease.
  • Further investigation into netarsudil for AD treatment is warranted.