Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Alzheimer Disease l: Introduction

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...

Aging

Aging

Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
Cellular Clock Theory
The cellular clock theory posits that the human lifespan is closely tied to the finite capacity of cells to divide, a phenomenon governed by telomeres, which are protective caps at the ends of...

Pharmacodynamics in Geriatric Patients: Effects of Age

Pharmacodynamics in Geriatric Patients: Effects of Age

Age-related pharmacokinetic changes are extensively documented, but understanding age-related pharmacodynamic alterations is relatively limited. This knowledge gap can be partly attributed to the complexity of developing appropriate measures of drug responses compared to bioanalytical methods for determining drug concentrations.Most information regarding age-related differences in human pharmacodynamics originates from cross-sectional studies. However, these studies assume that observed mean...

Alzheimer's Disease: Overview

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...

Alzheimer Disease ll: Pathophysiology

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...

Alzheimer's Disease: Treatment

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...

You might also read

Related Articles

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

Sort by

Same author

Leptin gene therapy attenuates neuronal damages evoked by amyloid-β and rescues memory deficits in APP/PS1 mice.

Gene therapy·2014

Same author

Specific roles for Group V secretory PLA₂ in retinal iron-induced oxidative stress. Implications for age-related macular degeneration.

Experimental eye research·2013

Same author

Differential participation of phospholipase A2 isoforms during iron-induced retinal toxicity. Implications for age-related macular degeneration.

Neurochemistry international·2012

Same author

Effect of transition metals in synaptic damage induced by amyloid beta peptide.

Neuroscience·2010

Same author

Biosynthesis of membrane lipids in the retina: Subcellular distribution and propranolol action on phosphatidic acid, phosphatidylserine and phosphatidylethanolamine.

Neurochemistry international·2010

Same author

Selective localization of phosphatidylcholine-derived signaling in detergent-resistant membranes from synaptic endings.

Biochimica et biophysica acta·2009

Same journal

Integrated single-cell and Mendelian randomization analyses identify aging-induced brain endothelial SPARCL1 deficiency as a key driver of vascular dementia.

Experimental gerontology·2026

Same journal

Effects of different intensities of aerobic exercise on intestinal permeability and inflammatory response in older adults: Randomized clinical trial.

Experimental gerontology·2026

Same journal

Gut microbial signature for frailty discrimination: a metagenomic meta-analysis of 28 independent cohorts.

Experimental gerontology·2026

Same journal

The joint association of biological aging and dietary oxidative balance score with cardiometabolic multimorbidity among U.S. older adults.

Experimental gerontology·2026

Same journal

Proanthocyanidins and skeletal muscle health: An integrative systematic review of molecular, preclinical, and clinical evidence.

Experimental gerontology·2026

Same journal

Time-dependent circulating metabolic changes and key regulatory pathways in Alzheimer's disease: A combined animal model and public database study.

Experimental gerontology·2026

See all related articles

Search research articles

Related Experiment Video

Updated: Apr 20, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Normal aging in rats and pathological aging in human Alzheimer's disease decrease FAAH activity: modulation by

A C Pascual¹, A M Martín-Moreno², N M Giusto¹

¹Instituto de Investigaciones Bioquímicas de Bahía Blanca, Universidad Nacional del Sur and Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), 8000 Bahía Blanca, Argentina.

Experimental Gerontology

|December 3, 2014

Summary

This summary is machine-generated.

Fatty acid amide hydrolase activity, crucial for endocannabinoid regulation, decreases in Alzheimer

Keywords:

Aging Alzheimer's disease Anandamide Cannabinoid receptors Central nervous system Fatty acid amide hydrolase

More Related Videos

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Published on: August 22, 2014

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

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: Apr 20, 2026

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Preparation of Acute Hippocampal Slices from Rats and Transgenic Mice for the Study of Synaptic Alterations during Aging and Amyloid Pathology

Published on: March 23, 2011

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Getting to Compliance in Forced Exercise in Rodents: A Critical Standard to Evaluate Exercise Impact in Aging-related Disorders and Disease

Published on: August 22, 2014

Establishment of a Valuable Mimic of Alzheimer's Disease in Rat Animal Model by Intracerebroventricular Injection of Composited Amyloid Beta Protein

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
Biochemistry
Pharmacology

Background:

Anandamide, an endocannabinoid, plays a role in neuroprotection.
Fatty acid amide hydrolase (FAAH) regulates anandamide levels by degrading it.
Understanding FAAH activity in aging and Alzheimer's disease (AD) is crucial.

Purpose of the Study:

To characterize anandamide breakdown via FAAH in physiological and pathological aging.
To investigate the regulation of FAAH activity by CB1 and CB2 receptor agonists.

Main Methods:

Analysis of FAAH activity in human cortical membranes (controls and AD patients).
Measurement of FAAH activity in rat cerebral cortex (adults and aged).
Assessment of agonist effects (JWH-133, WIN55,212-2) on anandamide hydrolysis.

Main Results:

FAAH activity decreased in the frontal cortex of AD patients, mimicked by Aβ(1-40) peptide.
FAAH activity showed differential changes in aged rat brain membranes and synaptosomes.
CB1/CB2 agonists differentially modulated anandamide hydrolysis in human AD and aged rats.

Conclusions:

Anandamide availability is reduced in Alzheimer's disease.
Anandamide availability is increased in physiological aging.
Differential modulation of FAAH by cannabinoid receptor agonists impacts anandamide levels in AD and aging.