Alzheimer’s disease (AD) is an age-related neurological disease that affects tens of millions of people, in addition to their carers. Hallmark features of AD include plaques composed of amyloid beta, as well as neurofibrillary tangles of tau protein. However, despite more than a century of study, the cause of Alzheimer’s disease remains unresolved. The roles of amyloid beta and tau are being questioned and other causes of AD are now under consideration. The contributions of researchers, model organisms, and various hypotheses will be examined in this Special Issue.

From the reviews: ""Brain Neurosecretory Cytokines is an excellent book, a veritable goldmine of information, at the cutting edge of neuroscience. It should stimulate ideas for future directions in neuroscience for years to come. This volume should be highly useful for medical libraries, neuroscientists, endocrinologists and graduate students in these fields."" (Arthur S. Brecher, TRENDS in Endocrinology & Metabolism, Vol. 16 (6), 2005)

The mechanistic target of rapamycin (mTOR) is a major signaling intermediary that coordinates favorable environmental conditions with cell growth. Indeed, as part of two functionally distinct protein complexes, named mTORC1 and mTORC2, mTOR regulates a variety of cellular processes, including protein, lipid, and nucleotide synthesis, as well as autophagy. Over the last two decades, major molecular advances have been made in mTOR signaling and have revealed the complexity of the events implicated in mTOR function and regulation. In parallel, the role of mTOR in diverse pathological conditions has also been identified, including in cancer, hamartoma, neurological, and metabolic diseases. Through a series of articles, this book focuses on the role played by mTOR in cellular processes, metabolism in particular, and highlights a panel of human diseases for which mTOR inhibition provides or might provide benefits. It also addresses future studies needed to further characterize the role of mTOR in selected disorders, which will help design novel therapeutic approaches. It is therefore intended for everyone who has an interest in mTOR biology and its application in human pathologies.

Redox homeostasis results from the balance between the production of reactive species (e.g. ROS, RNS, etc) and their detoxification by endogenous or exogenous antioxidants. ROS play several important physiological roles, however, their excessive production or impaired detoxification is associated with oxidative stress and cellular injury. Importantly, oxidative damage to vulnerable central nervous system (CNS) cells is a common pathological feature of several neurodegenerative diseases. Antioxidants have been considered as attractive potential therapeutic agents to prevent or halt disease progression but the clinical efficacy of antioxidant treatment strategies is still marginal. Improvement of antioxidant therapy effectiveness might involve adjustment of preclinical to clinical settings and development of new efficient delivery methods and will require a more in-depth knowledge of cellular redox-signaling mechanisms. Promising novel redox-based therapeutic strategies are gaining relevance to combat oxidative stress associated with neurodegenerative diseases. These include boosting the endogenous antioxidant machinery through activation of the antioxidant master regulator Nrf2 (nuclear factor erythroid 2-related factor 2) or modulation of ROS production by NOX (nicotinamide adenine dinucleotide phosphate (NADPH) oxidase) inhibitors. Redox regulation of key cellular functions is currently recognized as an important cellular signaling mechanism and events such as post-translational modifications (e.g. S_glutathionylation, S_nitrosylation, glycosylation, etc) play important roles in redox signal transduction and might be instrumental to uncover pathological mechanisms and identify novel therapeutic targets in neurodegenerative diseases. This Research Topic focuses on redox signaling mechanisms and aims to provide novel insights into the role of redox-signaling, with particular emphasis on redox regulation involving post-translational modifications, in the pathophysiology of neurodegenerative diseases. Moreover, it aims to present an overview of the potential of antioxidants as therapeutics for CNS disorders with a special focus on emerging novel therapeutic redox-based strategies. We are particularly interested in studies: -addressing new redox-based molecular mechanisms contributing to neurodegenerative diseases; -exploring the role of naturally occurring compounds, standard medications, and nutraceuticals with antioxidant properties in modulating redox-signaling pathways and limiting and/or preventing oxidative damage associated with these disorders; -addressing mechanistically the role of post-translational modifications in the pathophysiology of neurodegenerative disorders.