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

Glaucoma: Overview01:25

Glaucoma: Overview

Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...
Angle Closure Glaucoma: Treatment01:28

Angle Closure Glaucoma: Treatment

Angle-closure glaucoma, or closed-angle glaucoma, is an eye condition where the iris bulges out and blocks the iridocorneal angle, resulting in a buildup of aqueous humor and increased intraocular pressure. Immediate medical attention is necessary due to the sudden onset of symptoms. The treatment for angle-closure glaucoma includes short-term and long-term approaches. Short-term treatment involves using eye drops like pilocarpine to lower intraocular pressure by increasing aqueous humor...
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...
Open Angle Glaucoma: Treatment01:27

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...
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 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

Asymmetric Optic Disc Edema in Astronauts: A Narrative Review Proposing an Interplay Between Ocular Venous Congestion and Glymphatic Transport.

Life (Basel, Switzerland)·2026
Same author

Ocular Glymphatic Dysfunction as a Potential Link Between Obstructive Sleep Apnea and Retinal Structural Changes. Comment on Pusic Sesar et al. Multimodal Assessment of Ocular Parameters in Patients with Severe Obstructive Sleep Apnea with Emphasis on Retinal Structural Changes. <i>Life</i> 2025, <i>15</i>, 1307.

Life (Basel, Switzerland)·2026
Same author

An interpretable machine learning framework with data-informed imaging biomarkers for diagnosis and prediction of Alzheimer's disease.

Computerized medical imaging and graphics : the official journal of the Computerized Medical Imaging Society·2026
Same author

Cognitive correlates of cortical thickness, white matter volume, and resting-state connectivity in mild cognitive impairment.

Journal of Alzheimer's disease : JAD·2026
Same author

Limited evidence for heart rate variability as a predictor of cognitive and pathophysiological brain markers.

Journal of Alzheimer's disease : JAD·2025
Same author

Glymphatic transport and ocular diseases.

Progress in retinal and eye research·2025

Related Experiment Video

Updated: Jun 17, 2026

In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
12:48

In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma

Published on: May 11, 2015

Alzheimer's disease: cerebral glaucoma?

Peter Wostyn1, Kurt Audenaert, Peter Paul De Deyn

  • 1Department of Psychiatry, PC Sint-Amandus, Reigerlostraat 10, 8730 Beernem, Belgium. wostyn.peter@skynet.be

Medical Hypotheses
|January 9, 2010
PubMed
Summary

High intracranial pressure (ICP) may increase Alzheimer's disease (AD) risk. Recent findings suggest cerebrospinal fluid pressure variations in AD patients support this, drawing parallels between AD and glaucoma.

More Related Videos

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Using Retinal Imaging to Study Dementia
09:17

Using Retinal Imaging to Study Dementia

Published on: November 6, 2017

Related Experiment Videos

Last Updated: Jun 17, 2026

In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma
12:48

In Vivo Dynamics of Retinal Microglial Activation During Neurodegeneration: Confocal Ophthalmoscopic Imaging and Cell Morphometry in Mouse Glaucoma

Published on: May 11, 2015

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation
08:30

Glaucoma-inducing Procedure in an In Vivo Rat Model and Whole-mount Retina Preparation

Published on: March 12, 2016

Using Retinal Imaging to Study Dementia
09:17

Using Retinal Imaging to Study Dementia

Published on: November 6, 2017

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Pathophysiology

Background:

  • A 1994 hypothesis suggested elevated intracranial pressure (ICP) may predispose individuals to Alzheimer's disease (AD).
  • Cerebrospinal fluid pressure (CSFP) exhibits interindividual variability, with some individuals having characteristically high ICP.
  • The initial hypothesis proposed that this elevated ICP subgroup might be more susceptible to AD development.

Purpose of the Study:

  • To discuss recent research on CSFP in AD patients that may support the high ICP hypothesis for AD.
  • To explore the potential link between Alzheimer's disease and glaucoma, considering similarities in pressure-induced neuronal cell death.
  • To question whether AD could be conceptualized as a cerebral form of glaucoma.

Main Methods:

  • Review and interpretation of existing research findings on CSFP distribution in AD patients.
  • Comparison of cellular and anatomical similarities between the intraocular pressure (IOP) space in glaucoma and the ICP space in the brain.
  • Analysis of recent research on retinal ganglion cell death in glaucoma and neuronal cell death in AD.

Main Results:

  • Recent findings on CSFP in AD patients could be interpreted as supporting the hypothesis that high ICP is linked to AD.
  • Similarities in the mechanisms of neuronal cell death in glaucoma and AD have been identified.
  • Anatomical and functional parallels exist between the IOP and ICP spaces.

Conclusions:

  • The hypothesis linking high ICP to AD susceptibility warrants further investigation.
  • AD may share underlying mechanisms with glaucoma, potentially representing a cerebral manifestation of glaucomatous processes.
  • Further research is crucial to determine the role of elevated ICP in the pathogenesis of Alzheimer's disease.