Acetylcholinesterase Inhibitors May Improve Myelin Integrity

  title={Acetylcholinesterase Inhibitors May Improve Myelin Integrity},
  author={George Bartzokis},
  journal={Biological Psychiatry},
  • G. Bartzokis
  • Published 15 August 2007
  • Biology, Psychology
  • Biological Psychiatry
Remyelination: A Potential Therapeutic Strategy for Alzheimer's Disease?
Treatments that promote myelination contribute to the recovery of neuronal function and improve cognition and strategies targeting myelin impairment may provide therapeutic opportunities for patients with AD.
Cholinesterase inhibition: is there evidence for disease-modifying effects?
It is plausible that cholinesterase inhibition might contribute to disease modification, and the detection of putative disease-modifying effects may be most easily implemented in certain patient subpopulations, and genotyping studies suggest a particular role for BuChE.
Neuroglialpharmacology: Myelination as a shared mechanism of action of psychotropic treatments
Alzheimer's disease as homeostatic responses to age-related myelin breakdown
Does Myelin Play the Leading Role in AlzheimerâÂÂs Disease Pathology?
Current knowledge on the place of myelin in AD pathology and its interactions with As and tau pathology is reviewed and it is suggested that myelin pathology may precede As andTau pathologies in AD.
Small compounds mimicking the adhesion molecule L1 improve recovery in a zebrafish demyelination model
It is found that the selected compounds tacrine and duloxetine significantly improved remyelination in the peripheral and central nervous system of transgenic zebrafish following pharmacologically induced demyelinations.
Myelin imaging of the basal forebrain in first-episode psychosis
Using data from the Allen Human Brain Atlas, cholinergic nuclei showed significant enrichment for schizophrenia and depression-related genes and cell type markers of oligodendrocytes andCholinergic neurons, providing biological validity to the measures.
Brain tissue modifications induced by cholinergic therapy in Alzheimer's disease
The reduced connectivity in WM bundles connecting the hippocampi with the rest of the brain (fornix/cingulum) suggests a possible mechanism for the spread of AD pathology, partially driven by neurotrophic properties of acetylcholine replacement.
Promising Genetic Biomarkers of Preclinical Alzheimer's Disease: The Influence of APOE and TOMM40 on Brain Integrity
The present paper aims to extend on the mitochondrial influence in AD pathogenesis and proposes a TOMM40-induced disconnection of the medial temporal lobe and discusses the possibility of mitochondrial dysfunction being the earliest pathophysiological event in AD.


The model provides a rational biological framework for the development of novel, myelin-centered treatments that may have widespread efficacy across multiple disease states and could potentially be used in treating, delaying, or even preventing some of the most prevalent and devastating neuropsychiatric disorders.
The cholinergic pathology in Alzheimer's disease – discrepancies between clinical experience and pathophysiological findings
  • L. Frölich
  • Biology, Psychology
    Journal of Neural Transmission
  • 2002
Data show that there is a plasticity of the central cholinergic system in AD and that the positive clinical effects of AChE-I are to be weighted against possible detrimental effects on a pathophysiological level.
Nicotinic receptors in aging and dementia.
Activation of neuronal nicotinic acetylcholine receptors (nAChRs) has been shown to maintain cognitive function following aging or the development of dementia. Nicotine and nicotinic agonists have
Nicotinic Receptor Modulation for Neuroprotection and Enhancement of Functional Recovery Following Brain Injury or Disease
It is demonstrated that nicotine is not neuroprotective in all animal models of neurodegenerative disease; in fact, C57Bl/6 mice pretreated with nicotine have an increased sensitivity to 3‐nitropropionic acid, a neurotoxin used in mice to mimic some aspects of Huntington's disease.
The Cholinergic Hypothesis of Age and Alzheimer's Disease-Related Cognitive Deficits: Recent Challenges and Their Implications for Novel Drug Development
Cholinergic abnormalities may also contribute to noncognitive behavioral abnormalities as well as the deposition of toxic neuritic plaques in AD and cholinergic-based strategies will likely remain valid as one approach to rational drug development for the treatment of AD other forms of dementia.
Neurotransmitter-mediated regulation of CNS myelination: a review.
It is anticipated that a better understanding of the neurotransmitter-mediated neuronal oligodendroglial communication network opens prospects in the field of central nervous system (CNS) myelin repair, allowing the recruitment of the myelinating machinery that is known to remain present but quiescent in the CNS of multiple sclerosis patients.
Quantifying age-related myelin breakdown with MRI: novel therapeutic targets for preventing cognitive decline and Alzheimer's disease.
This myelin-centered model together with the technology that makes it possible to measure the trajectory of myelin breakdown provide a framework for developing novel treatments, as well as assessing efficacy of currently available treatments, intended to slow or reverse the breakdown process in both clinically healthy aswell as symptomatic populations.
A short review of cognitive and functional neuroimaging studies of cholinergic drugs: implications for therapeutic potentials
Summary. In the last 20 years a cholinergic dysfunction has been the major working hypothesis for the pharmachology of memory disorders. Cholinergic antagonists and lesions impair and different
Targeting acetylcholinesterase and butyrylcholinesterase in dementia.
New evidence for the roles of BuChE and AChE in symptom generation and rate of underlying disease progression in dementia is focused on, and it is argued that it may be appropriate to re-evaluate the place of ChE-Is in the treatment of dementia.