In-vitro and in-vivo studies of two-drug cocktail therapy targeting chemobrain via the Nrf2/NF-κB signaling pathway.

Today, we critically need alternative therapeutic options for chemotherapy-induced cognitive impairment (CICI), often known as chemo brain. Mitochondrial dysfunction and oxidative stress are two of the primary processes that contribute to the development of chemobrain. Therefore, the purpose of this study was to investigate how CoQ10 and berberine shield neurons from chemotherapy-induced damage in in-vitro studies and memory loss in vivo studies.

Drug-herb combination therapy in cancer management.

Cancer is the second leading cause of fatality all over the world. Various unwanted side effects are being reported with the use of conventional chemotherapy. The plant derived bioactive compounds are the prominent alternative medicinal approach for reduction of chemotherapy associated side effects.

Cellular and Mitochondrial Quality Control Mechanisms in Maintaining Homeostasis in Aging.

Aging is a natural process in all living organisms defined as destruction of cell function as a result of long-term accumulation of damages. Autophagy is a cellular house safeguard pathway that is responsible for degrading damaged cellular organelles. Moreover, it maintains cellular homeostasis, controls lifetime and longevity.

Crosstalk between anticancer drugs and mitochondrial functions.

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.

A Novel Approach to Refractory Epilepsy by Targeting Pgp Peripherally and Centrally: Therapeutic Targets and Future Perspectives.

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 antiepileptic drugs (AEDs) by multidrug resistance (MDR) transporters from the epileptogenic tissue or reduced sensitivity of drug in epileptogenic brain tissue.

Targeting S100B Protein as a Surrogate Biomarker and its Role in Various Neurological Disorders.

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 the calcium-binding domain associated with various neurological disorders through activation of the MAPK pathway, increased NF-kB expression resulting 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 the high expression of this protein directly targets astrocytes and promotes neuroinflammation.