Conclusions There is substantial evidence

that, the chronic inflammatory reaction in AD results in neuronal injury, ultimately leading to cognitive decline. Microglia activated by β-AP and cofactors such as M-CSF are likely to play a major role in generating neurotoxic agents in and around the neuritic plaque lesion. Many potential therapeutic agents that could ameliorate the inflammatory reaction in AD are available, including NOS inhibitors, agents that block the actions of proinflammatorycytokines, and antioxidants. NOS inhibitors with isoform Inhibitors,research,lifescience,medical specificity are currently under development and should soon be available for testing. Likewise, many anticytokine reagents are currently available, including older agents such as glucocorticoids, nonspecific nonsteroidal agents, and cytokine receptor Inhibitors,research,lifescience,medical antagonists, as well as newer agents such as low-molecular-weight cytokine inhibitors, convertase inhibitors, and highly specific cyclooxygenase inhibitors. However, recent, evidence using β-AP immunizations

and transgenic animals indicates that, the inflammatory response may Inhibitors,research,lifescience,medical also have a beneficial response in AD, possibly through catabolism of β-AP and other abnormal protein products.86 Therapeutic approaches to attenuating inflammation in AD may need to be precisely targeted to disrupt, deleterious aspects of the inflammatory response, while preserving beneficial effects. Selected abbreviations and acronyms AD Alzheimer’s Dasatinib disease β-AP Inhibitors,research,lifescience,medical beta-amyloid peptide GM-CSF gramdocyte-macrophage colony-stimulating factor IL-1 interleukin-1 M-CSF macrophage colony-stimulating factor MSR macrophage scavenger receptor NO nitric oxide NOS nitric oxide synthase ROS reactive oxygen species Notes Drs

Barbara Cordell, Philipp Kahle, Jared Tinklenberg, and Jerome Yesavage contributed to this work. Expert technical assistance was provided by Lan Yang and Nina Pascoe. Supported by grants from the selleck Ixazomib National Institute of Mental Health.
Alzheimer’s disease (AD) is a significant public health problem secondary to the increased life expectancy of the general population Inhibitors,research,lifescience,medical and a better appreciation of the socioeconomic consequences of the disease. It was defined GSK-3 by Alois Alzheimer in 1906 using criteria of progressive memory loss, disorientation, and pathological markers (senile plaques and neurofibrillary tangles). Initially it was assumed that AD was a rare condition, and later it was considered to be an inevitable consequence of aging. The stigma attached to aging and other factors delayed aggressive research into, and treatment of, patients with AD, but these misconceptions are fading away, and treatments, though initially modest in efficacy, are becoming available. In this paper we will review the diagnosis, etiology, genetics, epidemiology, course, and treatment of AD. Diagnosis and course The clinical manifestations of AD include disturbances in the areas of memory and language, visuospatial orientation, and higher executive function.