: Neurological disorders (ND) are the central nervous system (CNS) related complications originated by enhanced oxidative stress, mitochondrial failure and overexpression of proteins like S100B. S100B is a helix-loop-helix protein with calcium-binding domain associated to various neurological disorders through activation of MAPK pathway, increased NFkB expression results in cell survival, proliferation and gene up-regulation. S100B protein plays a crucial role in Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, Schizophrenia and epilepsy because high expression of this protein directly targets astrocytes and promote neuroinflammation. Under stressful conditions, S100B produces toxic effect mediated through receptor for advanced glycation end products (AGE) binding. S100B also mediate neuroprotection, minimize microgliosis and reduce the expression of tumor necrosis factor (TNF-alpha) but that are concentration-dependent mechanisms. Increased level of S100B useful for assessing release of inflammatory markers, nitric oxide and excitotoxicity dependent neuronal loss. The present review summarizes the role of S100B in various neurological disorders and potential therapeutic measure to reduce the prevalence of neurological disorders.

Chemotherapy is an important component of cancer treatment, which has side effects like vomiting, peripheral neuropathy, and numerous organ toxicity but the most significant outcomes of chemotherapy are cognitive impairment, which is mainly referred to as chemobrain or CICI (chemotherapy-induced cognitive impairment). It is characterized by difficulty with language, concentrating, processing speed, learning, and memory, as it affects the hippocampus areas of the brain. Mitochondrial dysfunction and oxidative stress are one of the major mechanisms causing chemobrain. The generation of reactive oxygen species (byproducts of oxidative phosphorylation) mainly occurs in mitochondria that play a prominent role in the induction of oxidative stress. The homeostasis of ROS in the mitochondria is maintained by mitochondrial antioxidant mechanism via enzymes like catalase, glutathione, and superoxide dismutase. Lungs and breast cancer are the two most common types of cancer, which are the most leading cancers in the world with about 4.18 million cases. In this review we exposed the current knowledge regarding chemotherapy-induced oxidative stress and mitochondrial dysfunction to cause cognitive impairment.We especially focused on the antineoplastic agent (ADRIAMYCIN, CYCLOPHOSPHAMIDE), platinum group agent CISPLATIN, antimetabolite agents (METHOTREXATE), and nitrogen mustard agent (CARMUSTINE) which increase oxidative stress and inflammatory markers in the PNS (peripheral nervous system) as well as the central nervous system. We also highlight the behavioural and functional changes in the brain.

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Abstract:: Refractory epilepsy is a type of epilepsy involving seizures uncontrolled by first or second-line anticonvulsant drugs at a regular therapeutic dose. Despite considerable growth in epileptic pharmacotherapy, one-third of the patients are resistant to current therapies. In this, the mechanisms responsible for resistant epilepsy are either increased expulsion of an-tiepileptic drugs (AEDs) by multidrug resistance (MDR) transporters from the epileptogenic tissue or reduced sensitivity of drug in epileptogenic brain tissue. The difficulty to treat refractory epilepsy is because of drug resistance due to cellular drug efflux, use of drug monotherapy, and subtherapeutic dose administration. Increased expression of Pgp is also responsible for resistance epilepsy or refractory epilepsy. Increase glutamate expression via inhibition of cyclooxygenase-II (COX-II) en-zyme also upregulate P-glycoprotein (Pgp) expression and augment instance of recurrent seizures. Peripheral and central in-hibition of Pgp is a powerful tool to control this drug resistance epilepsy. Drug resistance primarily involves multidrug re-sistance (MDR1) gene which is responsible for encoding P-glycoprotein (PgP1 or MDR1). Currently, there is no drug under clinical practice which inhibits MDR1. The present review cites some drugs like calcium channel blockers, COX-II inhibi-tors, and glutamate receptors antagonists that inhibit P-gp. The exploitation of these targets may emerge as a beneficial ap-proach for patients with drug-resistant epilepsy. The present review further highlights the mechanistic role of Pgp in drug-resistant epilepsy, glutamate role in drug efflux, and management approach.