Related Experiment Video
Updated: Jun 20, 2026
05:12
A Mouse Model for Vascular Cognitive Impairment and Dementia Based on Needle-guided Asymmetric Bilateral Common Carotid Artery Stenosis
Published on: November 22, 2024
Choline acetyltransferase activity in vascular dementia and stroke
Sally I Sharp1, Paul T Francis, Mark S J Elliott
1Wolfson Centre for Age-Related Diseases, Guy's Campus, London, UK.
Dementia and Geriatric Cognitive Disorders
|September 25, 2009
Summary
Cholinergic function declines in vascular dementia (VaD) with Alzheimer's disease (AD) but increases in infarct dementia. This study reveals distinct cholinergic alterations in cerebrovascular diseases, offering potential new therapeutic targets.
Area of Science:
- Neuroscience
- Neuropathology
- Cerebrovascular Diseases
Background:
- Cholinergic system alterations are not well-understood in cerebrovascular diseases.
- This study focuses on cholinergic function in stroke and vascular dementia (VaD).
Purpose of the Study:
- To investigate postmortem cholinergic function in patients with stroke and VaD.
- To compare cholinergic activity in different subtypes of VaD and Alzheimer's disease (AD).
Main Methods:
- Postmortem brain tissue analysis from 61 patients with stroke or VaD, 12 with AD, and 23 controls.
- Measurement of choline acetyltransferase (ChAT) activity in Brodmann areas (BA) 9 and 20/21.
Main Results:
- Reduced ChAT activity was observed in VaD patients with concurrent AD compared to controls.
- Infarct dementia patients showed a significant 27% increase in ChAT activity in BA9.
- No correlation was found between ChAT activity and cognitive function in VaD patients.
Conclusions:
- Loss of cholinergic function is specific to VaD patients with co-existing AD.
- A novel increase in cholinergic activity in infarct dementia suggests potential therapeutic avenues.
Related Concept Videos
01:22Alzheimer'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...
01:23Cholinergic Neurons: Neurotransmission
Cholinergic neurotransmission involves the synthesis and the release of acetylcholine (ACh) in order to transmit nerve impulses across the synapse. The process begins with the synthesis of acetyl CoA, a precursor for ACh, from ATP, acetate, and coenzyme A in the mitochondria. Choline, another vital precursor, is transported inside the neuron through choline transporters, including high-affinity choline transporter CHT1, low-affinity choline transporter CTL1, and lower-affinity choline...
01:22Dementia 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...
01:30Cognitive Enhancers: Cholinesterase Inhibitors and NMDA Receptor Antagonists
Cognitive enhancers, also known as "smart drugs," are substances used to enhance memory, mental alertness, and concentration. These can be natural or synthetic and improve cognition in conditions like Alzheimer's disease (AD) and other neurodegenerative diseases. Some common examples include caffeine, amphetamines, methylphenidate, modafinil, arecoline, donepezil, vortioxetine, and piracetam. These enhancers work on the principle of synaptic plasticity and altered circuit function. They...
01:23Alzheimer 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...
01:26Alzheimer'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...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...