Research reportInvestigations of neurotoxicity and neuroprotection within the nucleus basalis of the rat
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Multi-target design strategies for the improved treatment of Alzheimer's disease
2019, European Journal of Medicinal ChemistryCitation Excerpt :Cholinergic and glutamatergic neuronal systems influence each other through their joint dysfunction, and cholinergic deficits and glutamate-related excitotoxicity are central to AD pathology [84]. Excessive activation of NMDA receptor is implicated in the degenerative process of cholinergic neurons in AD, with the instance that neuronal decline caused by direct injection of NMDA into the rat basal forebrain generates reduced activity of choline acetyltransferase in the cortex [85]. Thus, the AChE and NMDA receptor multi-target strategy can affect the cholinergic and glutamatergic systems and is becoming an important idea because NMDA receptor antagonists can confront neurodegeneration and AChEIs can recover memory and cognition.
Cholinergic modulation of event-related oscillations (ERO)
2014, Brain ResearchCitation Excerpt :Cholinergic hypofunction has also been related to a number of cognitive disorders in humans including: the progressing memory deficits associated with aging, Alzheimer׳s disease (AD), Parkinson׳s disease, Down-syndrome, progressive supranuclear palsy, Jakob–Creutzfeld disease, Korsakoff׳s syndrome and traumatic brain injury (for review see Niewiadomska et al. (2009), Schliebs and Arendt (2011), Woolf (2006) and Woolf and Butcher, (2011)). Activity of the enzyme choline acetyl transferase (ChAT) is typically used as a marker for the loss of cholinergic neurons (Wenk et al., 1994a, 1994b). Although it has been suggested in AD that post-mortem assays of ChAT might not be representative of the extracellular levels of Ach and cholinergic neural activity, there have been significant validation of the functional loss of cholinergic neural activity using several biomarkers such as structural/amyloid imaging, cerebrospinal fluid measurements, and glucose positron emission tomography (Frings et al., 2013; Wirth et al., 2013).
Management of moderate to severe Alzheimer's disease: Focus on memantine
2011, Taiwanese Journal of Obstetrics and GynecologyCitation Excerpt :Of particular relevance to the clinical use of memantine are preclinical studies on the neurotoxic effects of glutamate in structures known to be affected in AD, such as the cholinergic nucleus basalis of Meynert (NBM, or nucleus basalis magnocellularis in rats) [12, 14]. In successive studies done by Wenk et al. (1994, 1995, 1997) [26–28], memantine, at a dose considerably lower than that which causes side effects, given i.p. before NMDA microinjection, produced dose-dependent protection and resulted in plasma levels similar to those in patients given therapeutic doses. In a T-maze alternation task, memantine pretreatment also proved useful in antagonizing the learning deficits induced by microinjection of NMDA into the NBM [12,14].
Memantine: a NMDA receptor antagonist that improves memory by restoration of homeostasis in the glutamatergic system - too little activation is bad, too much is even worse
2007, NeuropharmacologyCitation Excerpt :It is not always recognised that infusion of 20 mg/kg/d is not comparable with acute i.p. injection of the same dose. For example, Creeley et al. (2006) wrote “we chose 20 mg/kg as the initial dose because this is the dose that others have reported is effective in protecting the adult rat brain against excitotoxic neurodegeneration (Wenk et al., 1994; Misztal et al., 1996; Danysz et al., 1997; Chen et al., 1998).” The cited papers Wenk et al. (1994) and Misztal et al. (1996) all used infusion of 20 mg/kg/d which leads to maximal plasma level which are at least four times lower than the peak concentration achieved after a single i.p. administration of the same dose.
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