About this Research Topic
Epilepsy is one of the most common types of neurological disorders, characterized by spontaneous recurrent seizures. Epilepsy affects over 70 million people worldwide. Despite the introduction of over 25 standard antiepileptic drugs (AEDs), such as carbamazepine, valproate, and lamotrigine, seizures still cannot be well-controlled in approximately one-third of patients with epilepsy. On the other hand, psychiatric and neurological comorbidities, including anxiety, depression, cognitive disabilities, are relatively common and often co-exist in people with epilepsy. Similar to epilepsy itself, the management of these comorbidities is also an increasingly serious clinical problem lacking an optimal treatment strategy. There is increasing interest in alternative or complementary therapies for the treatment of epilepsy and its related psychiatric comorbidities.
Complementary and alternative therapies are the term for medical products and practices that are not part of standard medical care. Traditional complementary/alternative therapies, such as traditional Chinese medicine (TCM), are handed down from generation to generation. Traditional complementary/alternative therapies are usually clinically used in some specific areas, though most of them still need to be carefully assessed by optimally designed clinical trials. For example, we recently found that tetramethylpyrazine, the main bioactive alkaloid isolated from the Ligusticum chuanxiong Hort, has shown a dose-dependent anti-epileptogenic effect in mouse models. The anti-epileptogenic effect of tetramethylpyrazine increased with its dose range from 10 mg/kg to 50 mg/kg. Such dose-dependent concentration/dose-response data, lack for most complementary and alternative therapies investigated so far, thus further thorough studies may help to ensure that the therapies will be tested with full pharmacological rigor.
On the other hand, recent clinical trials or preclinical animal studies suggested novel complementary/alternative therapies for epilepsy, such as the use of optogenetic brain stimulation to treat epilepsy. By using optogenetic modulation, we previously found that selective activation of medial septum cholinergic neurons (but not glutamatergic or GABAergic [gamma-aminobutyric acidergic] neurons) significantly attenuated hippocampal seizures, which may provide a candidate target for optogenetic brain stimulation to treat epilepsy.
However, the effect of both novel and traditional complementary/alternative therapies still needs to be further evaluated, and their mechanisms are complex and waiting to carefully be assessed by adequate research.
This Research Topic focuses on the mechanisms of novel and traditional complementary and alternative therapies for epilepsy as well as psychiatric comorbidities of epilepsy. We are open to studies providing solid experimental evidence underlying the mechanisms at the neural circuit level.
Of note, to ensure that the therapies will be tested with full pharmacological rigor, concentration/dose-response data included in the investigations with relevant vehicles/placebo treatments is required.
We would like the following questions to be addressed:
(1) Which are the mechanisms of epilepsy-related complementary/alternative therapies in neural circuits?
(2) What are the main effective compounds or targeted molecules of epilepsy-related complementary/alternative therapies and their preliminary mechanisms?
Contributors will ensure there is rigorous detail concerning the pharmacological mechanisms of chemically identified key constitutive molecules.
Complementary and alternative therapies are the term for medical products and practices that are not part of standard medical care. Traditional complementary/alternative therapies, such as traditional Chinese medicine (TCM), are handed down from generation to generation. Traditional complementary/alternative therapies are usually clinically used in some specific areas, though most of them still need to be carefully assessed by optimally designed clinical trials. For example, we recently found that tetramethylpyrazine, the main bioactive alkaloid isolated from the Ligusticum chuanxiong Hort, has shown a dose-dependent anti-epileptogenic effect in mouse models. The anti-epileptogenic effect of tetramethylpyrazine increased with its dose range from 10 mg/kg to 50 mg/kg. Such dose-dependent concentration/dose-response data, lack for most complementary and alternative therapies investigated so far, thus further thorough studies may help to ensure that the therapies will be tested with full pharmacological rigor.
On the other hand, recent clinical trials or preclinical animal studies suggested novel complementary/alternative therapies for epilepsy, such as the use of optogenetic brain stimulation to treat epilepsy. By using optogenetic modulation, we previously found that selective activation of medial septum cholinergic neurons (but not glutamatergic or GABAergic [gamma-aminobutyric acidergic] neurons) significantly attenuated hippocampal seizures, which may provide a candidate target for optogenetic brain stimulation to treat epilepsy.
However, the effect of both novel and traditional complementary/alternative therapies still needs to be further evaluated, and their mechanisms are complex and waiting to carefully be assessed by adequate research.
This Research Topic focuses on the mechanisms of novel and traditional complementary and alternative therapies for epilepsy as well as psychiatric comorbidities of epilepsy. We are open to studies providing solid experimental evidence underlying the mechanisms at the neural circuit level.
Of note, to ensure that the therapies will be tested with full pharmacological rigor, concentration/dose-response data included in the investigations with relevant vehicles/placebo treatments is required.
We would like the following questions to be addressed:
(1) Which are the mechanisms of epilepsy-related complementary/alternative therapies in neural circuits?
(2) What are the main effective compounds or targeted molecules of epilepsy-related complementary/alternative therapies and their preliminary mechanisms?
Contributors will ensure there is rigorous detail concerning the pharmacological mechanisms of chemically identified key constitutive molecules.
Keywords: Neural Circuits, Epilepsy, Psychiatric Comorbidities, Complementary and Alternative Therapies, Neuropharmacology
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