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With the increasing proportion of the elderly population, neurodegenerative diseases such as dementia are becoming more prevalent worldwide. Vascular risk factors are considered significant targets for cognitive decline prevention. We reviewed the effect of cardiovascular risk factors on cognitive decline prevention in the elderly to evaluate the quantity and quality of evidence in managing the elderly population with cognitive decline. Data analysis was available from 25 studies that explored the effects of controlling cardiovascular risk factors on the risk of cognitive impairment. These risk factors include diabetes mellitus, high blood pressure, high cholesterol levels, and exercise and physical activity. The most positive evidence was found for exercise and physical activity. On the other hand, diabetes mellitus and cholesterol modifications showed no positive impact on cognitive function. Studies on hypertension control were incongruous. There is a need for large-sample, robust randomized clinical trials to provide sufficient evidence for the modification of various cardiovascular risk factors in preventing cognitive decline. [ABSTRACT FROM AUTHOR]

Introduction: Alexander disease is a heterogeneous group of diseases with various manifestations based on the age of disease onset. This rare leukodystrophy syndrome with mutations in the GFAP gene could present with developmental delay and seizure in the infantile form to ataxia and bulbar palsy in adulthood. However, psychiatric symptoms are not welldefined and are usually evaluated after disease diagnosis, not before disease investigations. Case Report: Our patient is a 52-year-old Iranian woman with a history of depression since 17 years ago, a suicidal attempt two years ago, and ingestion of a large amount of opium with the intention of suicide 2 months ago. She was presented with disorientation and probably a delirious state in the last interview. Eventually, in comprehensive investigations, white matter hyperintensity in MRI and leukodystrophy was diagnosed to determine the cause of these changes, we did a gene study, found whole exon deletion of the GFAP gene, and made a diagnosis of late-onset Alexander disease. Conclusion: Neurological-onset manifestation of Alexander disease, specifically late-onset form, is the most common clinical picture of disease and was seen in about 90% of patients, but psychiatric symptoms are not well-known, and psychiatric-onset disease was not described yet. Various gene mutations were described in late-onset Alexander disease; however, the large whole exon deletion which was revealed in our patient is a novel mutation and significantly needs to be explored. Here authors describe a late-onset Alexander disease with psychiatriconset symptoms and novel large exon deletion in the GFAP gene. [ABSTRACT FROM AUTHOR]