Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology

Revett, Timothy J.; Baker, Glen B.; Jhamandas, Jack H.; Kar, Satyabrata

doi:10.1503/jpn.110190

Cited by 262 publications

(199 citation statements)

References 228 publications

(374 reference statements)

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“…However, glutamatergic neurotransmission was blocked in those experiments (Marrazzo et al, 2005). Glutamatergic transmission is a factor in Ab 25-35 -induced cell death, and elevated glutamate levels have been shown to induce Bax upregulation in neurons (Schelman et al, 2004, Revett et al, 2013. Thus, our data suggest that s receptor activation by afobazole can reduce Bax expression and concomitant cell death in the presence of Ab 25-35 even when glutamatergic transmission is not blocked.…”

Section: Discussionmentioning

confidence: 60%

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Behensky

Yasny

Shuster

et al. 2013

J Pharmacol Exp Ther

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Section: Discussionmentioning

confidence: 60%

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Behensky

Yasny

Shuster

et al. 2013

J Pharmacol Exp Ther

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“…The uncontrolled release of glutamate (neurotransmitter) contributes to inflammation and neuronal death. Neuroinflammation is also involved in the pathology of the AD as well the symptoms [10].…”

Section: Pathophysiologymentioning

confidence: 99%

Genetic Disorder Alzheimer

Rani

Singh

Arjuna

et al. 2017

Asian J Pharm Clin Res

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Alzheimer's disease (AD), slowly continuous neurological disorder, mostly appears in older >65 age that deals with the memory loss due to death or damage of brain cells and cognitive functions (thinking, reasoning, and behavior abnormalities) due to the accumulation of the specific protein (betaamyloid protein) which form plaque and fibers (tau tangles) in the brain. Not only the genetic factors are responsible but also most of the non-genetic factors are responsible for AD. Several mutations in the gene (APP, APOE, PENS1, PENS2 on chromosome no. 21, 19, 14, 1) are responsible for causing four types of AD. Memory loss is most common sign of AD. Predisposing factors of AD are hereditary, severe brain injury or traumatic, and metabolic diseases such as diabetes mellitus, hypercholesteremia, and obesity. Although treatment can manage some symptoms in few people, but there is no current mechanism to cure AD or stop its progression. Beta-secretase inhibitor molecule prevents the first step in a chain accumulation which leads to the formation of amyloid plaque in the brain. However, the scientist or researchers have established a compound NIC5-15 they have been found NIC5-15 has safe and effectual treatment which has been used to stabilize cognitive performance in patients with mild to moderate AD.

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“…Thus, some drugs have been tested in an attempt to modulate NMDA receptors so that they can decrease the formation of amyloid-β plaque and NFTs in AD. 25,48,49 D-cycloserine is an antibiotic capable of modulating the activity of NMDA receptors. It is capable of improving memory and cognitive processes.…”

Section: D-cycloserine and Nitromemantinementioning

confidence: 99%

Perspectives for treating Alzheimer's disease: a review on promising pharmacological substances

et al. 2016

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CONTEXT AND OBJECTIVE: Dementia is a syndrome characterized by functional and cognitive decline. Alzheimer's disease (AD) is one of the most common causes of dementia and has high prevalence among the elderly. It is known that there is no drug capable of interfering with the course of the disease. Research on treatments for AD has been marked by the appearance of new drugs and their abandonment. This study aimed to describe drugs that have been studied with regard to treating AD and which are capable of influencing the course of the disease. DESIGN AND SETTING: Narrative review on original articles published worldwide. METHODS: A systematized search was conducted in the PubMed/MEDLINE, Cochrane Library/Cochrane and SciELO/Bireme databases. The descriptors "Molecular Mechanisms of Pharmacological Action" and "Drug Therapy" were each combined with the descriptor "Alzheimer disease". All of these can be found in MeSH and DeCS. These descriptors were used alone or in combination, and a filter specifying publication between January 2009 and October 2015 in English, Spanish or Portuguese was set. RESULTS: 6,888 articles were found, of which 37 were included in this review; 70.3% of the articles selected were of good quality with low or unclear risk of bias. 86 drugs were considered promising for AD treatment and these were classified into 20 pharmacological categories. CONCLUSION: There are no drugs capable of influencing the course of AD such that treatments are safe and effective. However, immunomodulators stood out as promising, given their effectiveness and quality in the articles analyzed. RESUMO CONTEXTO E OBJETIVO:A demência é uma síndrome caracterizada por declínio funcional e cognitivo, sendo a doença de Alzheimer (DA) uma das causas mais comuns e de alta prevalência em idosos. Sabe-se que não há medicamento capaz de interferir no curso da doença e as pesquisas para o tratamento da DA têm sido marcadas pelo surgimento e abandono de novas drogas. O objetivo deste estudo foi descrever as drogas capazes de influenciar o curso da DA que têm sido estudadas para o tratamento da doença.

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Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology

Cited by 262 publications

References 228 publications

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Genetic Disorder Alzheimer

Perspectives for treating Alzheimer's disease: a review on promising pharmacological substances

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Glutamate system, amyloid β peptides and tau protein: functional interrelationships and relevance to Alzheimer disease pathology

Cited by 262 publications

References 228 publications

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β25–35

Genetic Disorder Alzheimer

Perspectives for treating Alzheimer's disease: a review on promising pharmacological substances

Contact Info

Product

Resources

About

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35

Afobazole Activation of σ-1 Receptors Modulates Neuronal Responses to Amyloid-β_25–35