Current Issue: 2019  Archive: 2018   2017  

Special Issue

Alzheimer's Disease Research

Submission Deadline: September 25, 2019 (Open)               Submit Now

Guest Editor

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.


Manuscripts should be submitted online at by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. Papers will be published continuously (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website. Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are refereed through a peer-review process. Guidelines for authors and other relevant information for submission of manuscripts are available on the Instructions for Authors page. OBM Neurobiology is an international peer-reviewed Open Access monthly journal published by LIDSEN. Please visit the Instructions for Authors page before submitting a manuscript.

Planned Papers

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.