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Cyclic adenosine monophosphate (cAMP) is a second messenger of paramount biological importance, involved in the regulation of a significant number of cellular functions through the cAMP-dependent intracellular signal transduction pathways. The aim of this "Frontiers in Pharmacology" Research Topic was to attract contributions that highlight emerging ideas in the cAMP field that: (i) describe its role in cellular function and homeostasis, (ii) present the current approaches to its pharmacological manipulation, and (iii) clarify its central role in the development of more targeted therapeutic approaches toward a spectrum of diseases. The present collection of articles highlights, in a representative (but certainly not exhaustive) way, the research activity and emerging concepts in the field, while it also reveals the therapeutic potential that targeted pharmacological manipulation of intracellular cAMP levels could exert on a number of pathological conditions.
Pioneering studies conducted in the 1980’s laid the foundation for the hypothesis that axonal regeneration is limited by CNS myelin, and the identification of myelin-associated glycoprotein (MAG), Nogo, and oligodendrocyte myelin glycoprotein (OMgp) as inhibitors of neurite outgrowth firmly established myelin as a key factor in regenerative failure. Mechanistically, it has been shown that MAG, Nogo, and OMgp mediate inhibition by binding to either Nogo receptor (NgR) or paired immunoglobulin receptor B (PirB), and initiating a signaling cascade that culminates in the activation of RhoA. Since the discovery of these proteins, there has been tremendous interest in identifying compounds and molecular mechanisms that are capable of overcoming myelin-mediated inhibition. Many studies have focused on pharmacological antagonism of receptors and signaling intermediates, while others have sought to identify and enhance endogenous pro-regenerative pathways. The most notable example of the latter is the conditioning lesion effect, which led to the discovery of cyclic AMP’s ability to overcome inhibition by MAG and myelin. Many of the agents tested in these studies have been shown to promote axonal regeneration in vivo, and this research topic allows researchers to share information about new treatments that have been developed in both academia and industry. As we look toward the future, it is becoming increasingly clear that reversal of myelin-mediated inhibition alone will not be sufficient to produce functional recovery from spinal cord injury, and that other factors, such as astroglial scarring, the expression of chondroitin sulfate proteoglycans, neuronal cell death, and lack of neurotrophic support, must also be taken into consideration. Combinatorial approaches therefore hold a great deal of promise, and we hope to initiate a dialogue on how stem cell transplantation, chondroitinase ABC, gene therapy, growth-promoting agents, and other methods can be combined to optimize functional recovery. We introduce this topic in honor of the life and work of Dr. Marie T. Filbin (1955-2014). Through these articles, we highlight past achievements in the field, novel findings, unanswered questions and innovative ideas that we hope will lead to new advances in axonal regeneration.
Frontiers in Clinical Drug Research - Alzheimer Disorders is a book series concerned with Alzheimer's disease (AD), a disease that causes dementia, or loss of brain function. This disease affects parts of the brain that affect memory, thought, and language. Chapters in each volume focus on drug research with special emphasis on clinical trials, research on drugs in advanced stages of development and cure for Alzheimer’s disease and related disorders.