OBM Neurobiology is an international peer-reviewed Open Access journal published quarterly online by LIDSEN Publishing Inc. By design, the scope of OBM Neurobiology is broad, so as to reflect the multidisciplinary nature of the field of Neurobiology that interfaces biology with the fundamental and clinical neurosciences. As such, OBM Neurobiology embraces rigorous multidisciplinary investigations into the form and function of neurons and glia that make up the nervous system, either individually or in ensemble, in health or disease. OBM Neurobiology welcomes original contributions that employ a combination of molecular, cellular, systems and behavioral approaches to report novel neuroanatomical, neuropharmacological, neurophysiological and neurobehavioral findings related to the following aspects of the nervous system: Signal Transduction and Neurotransmission; Neural Circuits and Systems Neurobiology; Nervous System Development and Aging; Neurobiology of Nervous System Diseases (e.g., Developmental Brain Disorders; Neurodegenerative Disorders).
OBM Neurobiology publishes research articles, technical reports and invited topical reviews. Although the OBM Neurobiology Editorial Board encourages authors to be succinct, there is no restriction on the length of the papers. Authors should present their results in as much detail as possible, as reviewers are encouraged to emphasize scientific rigor and reproducibility.
Alzheimer's Disease Research
Submission Deadline: September 25, 2019 (Open) Submit Now
Md. Golam Sharoar, PhD
Department of Neurosciences, University of Connecticut Health Center, 263 Farmington Ave, Farmington, CT 06030, USA
E-Mail: [email protected]
Research Interest: Alzheimer’s Disease; Neurodegeneration; Amyloid beta; Dystrophic neurites
About This Topic
Alzheimer's disease (AD) is a chronic neurodegenerative disease that usually starts slowly and worsens over time. The most common early symptom is difficulty in remembering recent events (short-term memory loss). It is the cause of 60–70% of cases of dementia. As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self-care, and behavioural issues. There is no treatment that cures Alzheimer's disease or alters the disease process in the brain. Affected people increasingly rely on others for assistance, often placing a burden on the caregiver; the pressures can include social, psychological, physical, and economic elements. This special issue will seek to address topics related to the causes and complications of AD, how other aspects of risk factors (e.g., lifestyle) may influence AD, and discuss interventions/solutions to prevent AD.
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Title: Insights in brain signal transduction can provide potential molecular targets to approach and manage Alzheimer’s disease
Author: Vincenza Rita Lo Vasco
Affiliation: Experimental and Clinical Medicine Department, University of Florence, Largo Brambilla 3, 50134 Florence
Mechanisms leading to neuronal cell death in human pathology are far to be fully delineated. Understanding the molecules involved in neuronal death and the timing of their recruitment might help to explain the natural history of degenerative processes, including the morphology abnormalities observed in Alzheimer’s disease (AD). Moreover, it might help refine the diagnosis defining molecular markers and find effective therapies, with special regard to slow cognitive deficit features, often associated with neurodegenerative diseases. Disturbances in signal transduction in neurons were supposed to underlie human cognitive decline. Different signal transduction pathways were analyzed in AD, offering interesting insights in the etiopathogenesis and promising therapy perspectives. As an example, AD is associated with abnormal neuronal Ca2+ homeostasis, and involvement of signal transduction pathways acting upon Ca2+ metabolism and phosphorylative regulation of proteins was described. Understanding role and timing of action of the signaling pathways recruited during the brain morphology changes in AD progression might help elucidate the aetiopathogenesis of the disease, paving the way to early diagnosis, prognosis refinement and/or novel molecular therapeutic strategies. Different signal transduction pathways probably involved in AD pathogenesis will be discussed in the present review.