Subacute Combined Degeneration

Neuroimaging Features of Acquired Metabolic and Toxic Encephalopathies

Background: Toxic and metabolic encephalopathies are easily misinterpreted or overlooked in daily neuroimaging practices.

Aims: This review aims to summarize the imaging features of a number of acquired metabolic and toxic encephalopathies.

Discussion: These conditions are not diagnosed easily. Imaging is very important in terms of diagnosis, assessment of treatment response and prediction of prognosis. Therefore, it is important for radiologists to know the imaging features of relatively frequent acquired metabolic and toxic encephalopathies.

Conclusion: Integration of clinical information with the MRI findings can help physicians in diagnosis and treatment of the underlying disease.

Pernicious Anemia: Fundamental and Practical Aspects in Diagnosis

Background: Pernicious Anemia (PA), the most common cause of cobalamin deficiency anemia worldwide, is an autoimmune disease of multifactorial etiologies involving complex environmental and immunological factors. Although it was first reported by Addison in 1849 with subsequent advances in understanding of pathogenesis and molecular biology, diagnosis of PA is still challenging for clinicians because of its complexity and diverse clinical presentations.

Conclusion: Herein, we provide an overview of PA, mainly focusing on its scientific and practical aspects in diagnosis. We also discuss the limitations of currently available diagnostic tools for the evaluation of cobalamin deficiency and PA.

Metformin: Repurposing Opportunities for Cognitive and Mood Dysfunction

Background: Cognitive deficits differentially affect individuals with type 2 diabetes mellitus (T2DM) and mood disorders. Accumulating evidence implicates disturbances in metabolism as salient to cognitive function. Thus, the mitigation of metabolic disturbances may preserve or ameliorate cognitive function. This review aims to evaluate available evidence investigating the effects of metformin on cognitive function as well as summarize putative mechanistic properties related to these clinical effects.

Methods: A PubMed search was conducted using the search words including, but not limited to: metformin, Major Depressive Disorder, type 2 diabetes mellitus, and cognitive dysfunction. All English language articles published from 1990 to July 2014 were reviewed.

Results: Extant preclinical and clinical data have been mixed, wherein both cognitive disruption and pro-cognitive effects have been reported with the administration of metformin. Sound mechanistic evidence supports metformin as a treatment; however, the heterogeneity of study designs has contributed to an inability to arrive at an unequivocal conclusion regarding metformin effects upon cognition.

Conclusion: Available evidence does not provide a robust signal for improvement in cognition in either mood disorder or T2DM samples. Notwithstanding, it is premature to label metformin as a “no-go” agent for further testing and development for cognitive dysfunction. A well designed, proof-of-concept trial of metformin investigating its possible cognitive effects in mood disorders is therefore warranted.

Epigenetics in Alzheimers Disease: a Focus on DNA Modifications

Epigenetic alterations have been associated with several human diseases including Alzheimers disease (AD). AD is a complex neurodegenerative disease characterized by a progressive decline in cognitive functions, neuronal cell loss and by the presence of β amyloid (Aβ) plaques and neurofibrillary tangles (NFTs) in the cortex. Mutations in specific genes have been identified but can only explain a small percentage of the AD cases. The origins of the sporadic cases of AD are still not known but there is evidence for a role of epigenetics in the etiology of the disease. In this review we focus on discussing the roles of DNA methylation and hydroxymethylation in the development and potential treatment of AD. We discuss papers showing that there are alterations in methylated cytosine (5mC) levels in AD and also highlight the potential role of hydroxylated methylcytosine (5hmC) in the epigenetic regulation of brain gene expression and perhaps in AD. We discuss the potential influence of environmental factors, working through epigenetic mechanisms, on increasing the risk of developing AD and their potential in treating this major neurodegenerative disorder.