Cesses, and as a result their therapeutic targets need to be distinctive. Ictogenesis describes the processes of transition in the interictal state to a seizure, whereas epileptogenesis is definitely the course of action by which a particular group or neuronal circuit becomes hyperexcitable, becoming in a BMS-8 Data Sheet position to spontaneously generate epileptic seizures. Advances inside the information with the genetics and pathophysiology of some precise ailments linked with epilepsy have led to the improvement of particular treatments for some syndromes, which include everolimus in tuberous sclerosis complicated [103] or lysosomal enzyme replacement in neuronal ceroid lipofuscinosis [104]. Nonetheless, and particularly in adult-onset epilepsy, there are actually nevertheless many kinds of epilepsy and epileptic syndromes of which the precise etiopathogenesis is unknown, and hence you will discover presently no precise therapeutic agents for those groups of individuals. Interestingly, the prospective bidirectional association of epilepsy and neurodegenerative processes opens the door towards the improvement of new molecular targets that could potentially enable modifying the course of epilepsy. Despite the fact that some ASDs have been shown to possess prospective antiepileptogenic properties in animal models, such effects haven’t been confirmed in larger clinical studies [105]. Furthermore, a prospective antiepileptogenic effect of many approved drugs, which includes atorvastatin, ceftriaxone, losartan, isoflurane, N-acetylcysteine, anakinra, rapamycin, and fingolimod, has been described in animal models [10612]. Despite the fact that the repositioning of these drugs could represent an appealing alternative in some distinct etiologies, these benefits haven’t been confirmed by clinical trials [113]. This effect may be explained by the truth that most experimental studies on epileptogenesis have already been strongly influenced by the kindling model, along with the evidence supporting the existence of kindling in humans is controversial [114]. Most of these studies are based on post-traumatic or post-stroke epilepsy, which Methyl jasmonate Technical Information represents the archetype of epileptogenesis secondary to identifiable acquired brainPharmaceuticals 2021, 14,15 ofinjury. It’s likely that the wide wide variety of etiologies, and the likely diverse mechanisms of epileptogenesis in other epilepsy syndromes, could have contributed for the difficulties in translating preclinical studies into clinical trials [113]. 4. Antiseizure Drugs in Neurodegenerative Diseases Due to the molecular hyperlinks amongst epilepsy as well as other neurodegenerative diseases, various studies have been carried out to evaluate the therapeutic potential of anticonvulsant drugs in these pathologies and also the therapeutic method to epilepsy as a comorbidity. The wide wide variety of anticonvulsant drugs and their various mechanisms of action have positioned this group of drugs as very intriguing candidates for those pathologies with the central nervous program with an uncertain origin or an inefficient accessible remedy. Nevertheless, the prospective neuroprotective role of those drugs in these pathologies remains unknown. 4.1. ASDs in Alzheimer’s Disease In AD, some authors have tried to elucidate the pharmacological possible of ASDs within the pathological improvement of AD. For instance, the analysis group of Dr. Mucke evaluated the impact of chronic therapy of levetiracetam (LEV) inside the hAPP mice model, which has abnormally high amounts of human A and displays abnormal neuronal network activity and epileptic seizures [115]. The authors discovered t.