Books by Kanwaljit Chopra

Depression is one of the most prevalent and life-threatening forms of mental illnesses associated with significant disability and mortality. Stress can be considered as a major contribution for the development of depressive disorder due to dysregulation of HPA-axis. Although there are multiple pathways that are involved in the pathogenesis of depression, the current antidepressants mainly target monoaminergic pathway. However, therapeutic potential of other pathways is still under investigation. Drugs targeting nitric oxide, cytokines and kynurenine acid pathway might be the drugs of choice in near future. Alzheimer¿s disease is a neurodegenerative disorder with progressive dementia. Although basic research in Alzheimer¿s disease has made remarkable progress in past 2 decades, currently available drugs are able to improve cognitive symptoms temporarily, and no treatment can reverse, stop, or even slow this inexorable neurodegenerative process. This book dwells on the recently unravelled pathogenetic hypothesis and therapeutics of mental depression and Alzheimer¿s disease.

Diabetes mellitus produces numerous neurophysiological & structural changes in the central and peripheral nervous system and it further leads to development of neuropathic pain & moderate cognitive deficits in diabetics. The etiology of diabetes associated neuropathic pain & cognitive decline is multifactorial and involves an underlying phenomenon of metabolic memory. The concept of ¿metabolic memory,¿ that is of diabetic vascular stresses persisting even after stringent glucose control, has been supported both in the laboratory and in the clinic in both type 1 & type 2 diabetes. Therefore, ¿switching off¿ the metabolic memory, could be an important strategy for the prevention of diabetic neurological complications. Insulin alone reverses the hyperglycemia but partially reversed neuropathic pain and memory deficits in diabetic rats. However, insulin in combination with tocotrienol, lycopene and sesamol not only attenuates the diabetic condition but also reverses neuropathic pain and memory loss by switching off various components of metabolic memory phenomenon. Thus, these interventions may find clinical application in therapeutic armamentarium of diabetics.