Modulation of Tau Neuronal Expression Induced by NMDA, non-NMDA and Metabotropic Glutamate Receptor Agonists

Couratier, P.; Sindou, Philippe; Tabaraud, F; Diop, Amadou Gallo; Spencer, Peter S.; Hugon, J.

doi:10.1006/neur.1995.0004

Cited by 18 publications

(10 citation statements)

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“…Indeed, previous reports support this notion and glutamatergic transmission is severely altered by early degeneration of corticocortical connections and hippocampal projections in AD [5]. In addition, glutamatergic neurons are prone to develop neurofibrillary tangles [6] and glutamate increases the expression and phosphorylation of tau [7][8][9].…”

Section: Introductionsupporting

confidence: 51%

Differential Regulation of Glutamate Receptors in Alzheimer’s Disease

et al. 2002

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Selective neurodegeneration is a prominent feature in Alzheimer’s disease; however, the mechanism of neuronal death is still unclear. Nonetheless, the topographical distribution of different types of receptors is thought to contribute to the regional selective nature of neuronal degeneration. Specifically, since glutamatergic transmission is severely altered by the early degeneration of cortico-cortical connections and hippocampal projections in Alzheimer’s disease, we suspect that glutamate receptors may play a new role in the pathophysiology of disease. Here we review the salient aspects of glutamate receptor expression in Alzheimer’s disease and how their differential regulation can contribute to the selective neurodegeneration seen in the disease. Additionally, we assess the potential therapeutic value of glutamate receptors as a target for drug intervention in Alzheimer’s disease.

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Section: Introductionsupporting

confidence: 51%

Differential Regulation of Glutamate Receptors in Alzheimer’s Disease

et al. 2002

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“…Finally, in vitro studies have provided evidence that glutamate toxicity may induce changes in tau phosphorylation similar to those observed in AD. Hence, phosphorylated tau levels were increased in primary rat neurons degenerating in response to acute or chronic treatment with toxic concentrations of NMDA (Couratier et al 1995(Couratier et al , 1996. Furthermore, acute treatment of human NT2 neurons (which express the NR1 NMDA subunit and mGluR1α subtype) with toxic NMDA induced an increase in the levels of phosphorylated tau; this effect was prevented by co-treatment with 1S,3R-ACPD (mGluR agonist; Paterlini et al 1998).…”

Section: Involvement Of Phospholipase a 2 In Inflammationmentioning

confidence: 96%

Cholinergic and glutamatergic alterations beginning at the early stages of Alzheimer disease: participation of the phospholipase A2 enzyme

Schaeffer

Gattaz

2008

Psychopharmacology

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“…Experimental findings indicate that in Alzheimer's disease there is an increase in either glutamate (decrease of uptake and/or increase of release) or other endogenous glutamate receptor agonists in the vicinity of neurons [11][12][13][14][15][16][17], and additionally -amyloid peptide either activates NMDA receptors themselves or enhances their sensitivity [18][19][20][21][22][23][24]. The activation of NMDA receptors enhances production of elements implied in the pathology of Alzheimer's disease such as -amyloid or tau protein [25][26][27][28][29]. This is supported by the finding that in vitro glutamate toxicity is blocked by antisense of tau mRNA [28] and in vivo excitotoxicity increases amyloid precursor protein (APP) production in glia [29].…”

Section: The Glutamatergic Hypothesismentioning

confidence: 97%

Memantine: A Therapeutic Approach in Treating Alzheimers and Vascular Dementia

Koch¹,

Uyanık²,

Fischer-Barnicol

2005

CDTCNSND

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Memantine has been clinically used in the treatment of organic disorders in Germany for over ten years and has now been approved in Europe and also in the US for moderate to severe Alzheimer's disease. The rationale for this indication is strongly related to the physiological and pathological role of glutamate in neurotransmission. Glutamate is an agonist of NMDA, kainate and AMPA (ionotropic) receptors, where its influence on NMDA receptors plays an important role with regard to neuronal plasticity effecting memory and learning. Excessive levels of glutamate result in neurotoxicity, in part by overactivation of NMDA receptors. Memantine acts as an uncompetitive antagonist of NMDA receptors and therefore compensates for this overactivation. Furthermore, memantine is a neuroprotective agent in various animal models based on both neurodegenerative and vascular processes, as it ameliorates cognitive and memory deficits. Memantine was effective and safe in several clinical studies, particularly in Alzheimer's disease. The compound is completely absorbed after oral intake and undergoes little metabolism. Having a low probability for drug-drug interactions, memantine, in principle, is suited for elderly patients exposed to multiple therapeutic therapies.

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Modulation of Tau Neuronal Expression Induced by NMDA, non-NMDA and Metabotropic Glutamate Receptor Agonists

Cited by 18 publications

References 0 publications

Differential Regulation of Glutamate Receptors in Alzheimer’s Disease

Differential Regulation of Glutamate Receptors in Alzheimer’s Disease

Cholinergic and glutamatergic alterations beginning at the early stages of Alzheimer disease: participation of the phospholipase A2 enzyme

Memantine: A Therapeutic Approach in Treating Alzheimers and Vascular Dementia

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