The cholinergic hypothesis of geriatric memory ..
Accordingly, although there ispresently no "cure" for Alzheimer's disease, a large number ofpotential therapeutic interventions have emerged that are designed tocorrect loss of presynaptic cholinergic function.
Beyond the Cholinergic Hypothesis: Do Current Drugs …
This article examines the existing scientific applicability of the original cholinergic hypothesis of Alzheimer's disease bydescribing the biochemical and histopathological changes of neurotransmitter markers that occur in the brains of patients withAlzheimer's disease both at postmortem and neurosurgical cerebralbiopsy and the behavioural consequences of cholinomimetic drugs andcholinergic lesions.
Accordingly, although there is presently no "cure" for Alzheimer's disease, a large number of potential therapeutic interventions have emerged that are designed to correct loss of presynaptic cholinergic function.
The Cholinergic Hypothesis of Cognitive Aging …
Trazodone, a phenylpiperazine–triazolopyridine antidepressant, was originally discovered and developed in Italy in the 1960s by Angelini research laboratories. This agent was developed according to the mental pain hypothesis, which was postulated from studying patients and which proposes that depression is associated with a decreased pain threshold . In contrast to other antidepressants available at the time of its development, trazodone demonstrated minimal effects on muscarinic cholinergic receptors.
Dilsaver noted that the cholinergic hypothesis should more ..
Cognitive impairments are among the most common neuropsychiatric sequelae of traumatic brain injury at all levels of severity. Cerebral cholinergic neurons and their ascending projections are particularly vulnerable to acute and chronic traumatically mediated dysfunction. In light of the important role of acetylcholine in arousal, attention, memory, and other aspects of cognition, cerebral cholinergic systems contribute to and may also be a target for pharmacologic remediation among individuals with post-traumatic cognitive impairments. This article will review the evidence in support of this hypothesis. Evidence of relatively selective damage to cholinergic injury, the development of persistent anticholinergic sensitivity, and the effects of cholinergic augmentation on memory performance are presented first. Thereafter, neuropathologic, electrophysiologic, and pharmacologic evidence of cholinergic dysfunction after traumatic brain injury in humans is reviewed. Finally, future directions for investigation of the cholinergic hypothesis and possible clinical applications of this information are discussed.