Glutamate receptors, neurotoxicity and neurodegeneration

Lau, Anthony; Tymianski, Michael

doi:10.1007/s00424-010-0809-1

Cited by 1,000 publications

(754 citation statements)

References 233 publications

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“…Glutamate receptors, particularly NMDA receptors, are involved in the pathophysiology of AD [64]. Excessive glutamate activity resulting in excessive calcium influx activates a number of enzymes including phospholipases, endonucleases, neuronal nitric oxide synthase and proteases that can result in neuronal toxicity leading to several neurodegerative diseases including AD [64].…”

Section: Other Possible Mechanisms Of Melatonin's Action In Alzheimermentioning

confidence: 99%

“…Excessive glutamate activity resulting in excessive calcium influx activates a number of enzymes including phospholipases, endonucleases, neuronal nitric oxide synthase and proteases that can result in neuronal toxicity leading to several neurodegerative diseases including AD [64]. Melatonin, by reducing the NMDA-induced high Ca 2+ influx, thereby offers a neuroprotective effect.…”

Section: Other Possible Mechanisms Of Melatonin's Action In Alzheimermentioning

confidence: 99%

“…The regulation of intracellular Ca 2+ by melatonin is explained through its action on melatonin MT2 receptors. cAMP -dependent protein kinase (PKA) is involved in the activation of calcium channels [64]. Melatonin, by acting through MT2 receptors, decreases cAMP formation and [65].…”

Section: Other Possible Mechanisms Of Melatonin's Action In Alzheimermentioning

confidence: 99%

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Alzheimer’s Disease: Focus on the Neuroprotective Role of Melatonin

Srinivasan¹

2012

J Neurol Res

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Alzheimer's disease (AD) is characterized by a progressive loss of memory and cognitive function, and by behavioural and sleep disturbances, including insomnia. The pathophysiology of AD has been attributed to oxidative stress-induced amyloid-β protein (Aβ) deposition. Abnormal tau protein, mitochondrial dysfunction and protein hyper-phosphorylation have been demonstrated in neural tissues of AD patients. AD patients exhibit severe sleep-wake disturbances and these sleep disturbances are associated with rapid cognitive decline and memory impairment. Optimally effective management of AD patients will likely require a drug that can arrest Aβ -induced neurotoxic effects and can also restore the disturbed sleep-wake rhythm, with improvement in sleep quality. In this context, the pineal hormone melatonin has been demonstrated to be an effective antioxidant that can prevent Aβ -induced neurotoxic effects through a variety of mechanisms. Sleep deprivation itself produces many effects including oxidative damage, impaired mitochondrial function, neurodegenerative inflammation, altered proteosomal processing and abnormal activation of enzymes. In addition to treating the signs and symptoms of AD, treatment of sleep disturbances may also be necessary for preventing and arresting AD progression. Besides melatonin, a number of melatonergic agonists such as ramelteon, agomelatine and tasimelteon are now used clinically for treating insomnia and other sleep disorders. Their use may also be beneficial in treating Alzheimer's disease.

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Section: Other Possible Mechanisms Of Melatonin's Action In Alzheimermentioning

confidence: 99%

Section: Other Possible Mechanisms Of Melatonin's Action In Alzheimermentioning

confidence: 99%

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Alzheimer’s Disease: Focus on the Neuroprotective Role of Melatonin

Srinivasan¹

2012

J Neurol Res

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“…Acetylcholine deficiency has been reported in the disease profiles of AD, PD, and Myasthenia Gravis [14]. Another neurotransmitter glutamate, has an essential role in learning and memory related functions [15,16].…”

Section: Introductionmentioning

confidence: 99%

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Choudhury¹,

Sahu²,

Ramanujam³

et al. 2018

Neuropsychiatry

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Structural changes in different regions of the brain have become clinically relevant and regarded as the signature phenomenon for neurological diseases. Morphological changes in brain are also associated with neuronal and neurochemical alterations. Studies have showed that minute changes in neurochemical levels may have marked impact on the psychobehaviour of the subject. Several neurological disease profiles have been reported with such specific psychobehavioural expression. However, application of behavioural abnormalities as possible disease progress markers has not been considered and emphasised much. Reports suggested that-the subjects, who have already entered into the terminal stage of the disease, used to show cardinal behavioural signs for a specific disease profile. However, psychological expressions are comparatively early expressive. As most of the neurodegenerative disorders are unidirectional and progressive by nature, therapeutic intervention at the right time is essential for attaining the desired outcome. Moreover, early diagnosis can aid in managing the disease progression also. Psychobehavioural analysis could meet the expected outcome of disease diagnosis if implemented properly and timely. In the present review, we have amalgamated the reported behavioural anomalies with the supportive background from neurochemical basis. Further, we have concluded that behaviour centric studies could be a potential diagnostic tool for the early diagnosis of major neurological diseases such as Alzheimer disease, Parkinson's disease, Amyotrophic lateral sclerosis (ALS), Bipolar disorder, Schizophrenia, Impulse control disorder (ICD) and Obsessive-compulsive disorder (OCD).

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“…It is well established that during stroke, brain trauma and epilepsy neurons are transiently or permanently overloaded with Ca 2 + that could be detrimental (Lau and Tymianski, 2010). Therefore, we asked whether ER dynamics could be monitored in the living brain, and if rapid ER fragmentation occurs in a condition of neuronal Ca 2 + overload.…”

Section: Introductionmentioning

confidence: 99%

Rapid Fragmentation of the Endoplasmic Reticulum in Cortical Neurons of the Mouse Brain in situ Following Cardiac Arrest

Kucharz

Wieloch

Toresson

2011

J Cereb Blood Flow Metab

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Neuronal endoplasmic reticulum (ER), continuous from soma to dendritic spines, undergoes rapid fragmentation in response to N-methyl-D-aspartate (NMDA) receptor stimulation in hippocampal slices and neuronal primary cultures. Here, we show that ER fragments in the mouse brain following cardiac arrest (CA) induced brain ischemia. The ER structure was assessed in vivo in cortical pyramidal neurons in transgenic mice expressing ER-targeted GFP using two-photon laser scanning microscopy with fluorescence recovery after photobleaching (FRAP). Endoplasmic reticulum fragmentation occurred 1 to 2 minutes after CA and once induced, fragmentation was rapid ( < 15 seconds). We propose that acute ER fragmentation may be a protective response against severe ischemic stress.

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Glutamate receptors, neurotoxicity and neurodegeneration

Cited by 1,000 publications

References 233 publications

Alzheimer’s Disease: Focus on the Neuroprotective Role of Melatonin

Alzheimer’s Disease: Focus on the Neuroprotective Role of Melatonin

Neurochemicals, Behaviours and Psychiatric Perspectives of Neurological Diseases

Rapid Fragmentation of the Endoplasmic Reticulum in Cortical Neurons of the Mouse Brain in situ Following Cardiac Arrest

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