The therapeutic effect of quetiapine on cognitive impairment associated with 5-HT1A presynaptic receptor involved schizophrenia

Han, Dai Hoon; Shi, Sheng; Hong, Luo

doi:10.31083/j.jin.2019.03.186

Cited by 5 publications

(3 citation statements)

References 40 publications

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“…The present results suggest that the presynaptic function of 5-HT 1A receptors may be important for the inhibition of hyperactivity in DD mice. Previous studies demonstrated the importance of the presynaptic function of 5-HT 1A receptors rather than their postsynaptic functions for the treatment of a low level of social interaction, anxiety, and cognitive dysfunction [23,24]. Thus, presynaptic 5-HT 1A receptors may also play an important role in improving PSDD.…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Quetiapine and 5-HT1A Receptor Agonism on Hyperactivity in Dopamine-Deficient Mice

Ochiai

Fujita

Hagino

et al. 2022

IJMS

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Some diseases that are associated with dopamine deficiency are accompanied by psychiatric symptoms, including Parkinson’s disease. However, the mechanism by which this occurs has not been clarified. Previous studies found that dopamine-deficient (DD) mice exhibited hyperactivity in a novel environment. This hyperactivity is improved by clozapine and donepezil, which are used to treat psychiatric symptoms associated with dopamine deficiency (PSDD). We considered that DD mice could be used to study PSDD. In the present study, we sought to identify the pharmacological mechanism of PSDD. We conducted locomotor activity tests by administering quetiapine and drugs that have specific actions on serotonin (5-hydroxytryptamine [5-HT]) receptors and muscarinic receptors. Changes in neuronal activity that were induced by drug administration in DD mice were evaluated by examining Fos immunoreactivity. Quetiapine suppressed hyperactivity in DD mice while the 5-HT1A receptor antagonist WAY100635 inhibited this effect. The number of Fos-positive neurons in the median raphe nucleus increased in DD mice that exhibited hyperactivity and was decreased by treatment with quetiapine and 5-HT1A receptor agonists. In conclusion, hyperactivity in DD mice was ameliorated by quetiapine, likely through 5-HT1A receptor activation. These findings suggest that 5-HT1A receptors may play a role in PSDD, and 5-HT1A receptor-targeting drugs may help improve PSDD.

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Section: Discussionmentioning

confidence: 99%

Therapeutic Effects of Quetiapine and 5-HT1A Receptor Agonism on Hyperactivity in Dopamine-Deficient Mice

Ochiai

Fujita

Hagino

et al. 2022

IJMS

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“…It decreases the Bcl-XL/Bax ratio in the posterior cingulate cortex, ameliorating cognitive impairment and brain apoptotic processes. The drug has reached phase IV clinical trial [ 143 ]. Lecozotan, a selective 5HT1A receptor antagonist, shows increased learning and memory in rats by stimulating the release of glutamate and acetylcholine in the hippocampus [ 145 , 146 ].…”

Section: Neurobiology and Management Of Disease-associated Cognitive ...mentioning

confidence: 99%

Strategies for Treatment of Disease-Associated Dementia Beyond Alzheimer's Disease: An Update

Khan

Khatik

Datusalia

2023

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Memory, cognition, dementia, and neurodegeneration are complexly interlinked processes through various mechanistic pathways leading to a range of clinical outcomes. These are strongly associated with pathological conditions like Alzheimer’s disease, Parkinson’s disease, schizophrenia, stroke and are a growing concern for their timely diagnosis and management. Several cognition-enhancing interventions for management include non-pharmacological interventions like diet, exercise, and physical activity, while pharmacological interventions include medicinal agents, herbal agents, and nutritional supplements. This review critically analyzed and discussed the currently available agents under different drug development phase designed to target either of the molecular targets including cholinergic receptor, glutamatergic system, GABAergic targets, glycine site, serotonergic targets, histamine receptors, etc. Understanding memory formation and pathways involved therein aids in opening the new gateways to treating cognitive disorders. However, clinical studies suggest that there is still a dearth of knowledge about the pathological mechanism involved in neurological conditions, making the dropouts of agents from initial phases of clinical trial conducive. Hence, better understandings of the molecular basis of the disease biology, mode of drug action, and interlinked mechanistic pathways are required.

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“…In addition to the role of 5-HT 2A receptors in the treatment of cognitive deficit in schizophrenic patients, the role of other serotonin receptors has also been studied. Some atypical antipsychotic drugs, such as quetiapine or aripiprazole, stimulate 5-HT 1A receptors [135,136], providing an inhibitory feedback control of serotonin release in several areas of the brain [137]. This effect is related with an improvement in some cognitive functions such as verbal memory in schizophrenic patients, as seen with the 5-HT 1A agonist tandospirone [138].…”

Section: Modulation Of Serotonergic Neurotransmissionmentioning

confidence: 99%

Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments

Martínez

Brea

Rico

et al. 2021

IJMS

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Schizophrenia is a major mental illness characterized by positive and negative symptoms, and by cognitive deficit. Although cognitive impairment is disabling for patients, it has been largely neglected in the treatment of schizophrenia. There are several reasons for this lack of treatments for cognitive deficit, but the complexity of its etiology—in which neuroanatomic, biochemical and genetic factors concur—has contributed to the lack of effective treatments. In the last few years, there have been several attempts to develop novel drugs for the treatment of cognitive impairment in schizophrenia. Despite these efforts, little progress has been made. The latest findings point to the importance of developing personalized treatments for schizophrenia which enhance neuroplasticity, and of combining pharmacological treatments with non-pharmacological measures.

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The therapeutic effect of quetiapine on cognitive impairment associated with 5-HT1A presynaptic receptor involved schizophrenia

Cited by 5 publications

References 40 publications

Therapeutic Effects of Quetiapine and 5-HT1A Receptor Agonism on Hyperactivity in Dopamine-Deficient Mice

Therapeutic Effects of Quetiapine and 5-HT1A Receptor Agonism on Hyperactivity in Dopamine-Deficient Mice

Strategies for Treatment of Disease-Associated Dementia Beyond Alzheimer's Disease: An Update

Cognitive Deficit in Schizophrenia: From Etiology to Novel Treatments

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