Abstract
Editorial Alzheimer’s disease (AD) is a progressive neurological disorder, which represents the most common form of dementia, one of the major causes of disability in later life. Age is the greatest risk factor for AD, which typically affects people aged 65 years and over, with an age-standardised prevalence of 4.4 [1]. However, AD is not a normal part of ageing and advanced age alone does not justify the disease. Several pathways have been implicated in AD pathophysiology, the most described is the neurodegenerative one, which lead to the brain accumulation of beta-amyloid and neurofibrillary tangles, aggregations of hyperphosphorylated tau protein, macroscopically resulting in brain atrophy due to neuronal death [2]. These pathological hallmarks of AD have been recently incorporated in the new recommendations on diagnostic guidelines for AD, which describe different stages of the disease, including its preclinical and symptomatic pre-dementia phases [3]. Genetics accounts for less than 3% of AD, familiar AD at early onset, resulting from mutations in three genes, i.e. APP, PS1 and PS2. Furthermore, the Apolipoprotein E4 (ApoE4) genotype is the only, robust, susceptibility gene for AD [2], although meta-analysis and genome scanning have revealed several susceptibility loci with low odds ratios [4,5]. Overall, multiple gene-gene and environment interactions cause AD; however, various risk factors differently act throughout ageing [2,6]. Large data have been collected in the last two decades regarding the putative role of vascular disease, including systemic atherosclerosis, high blood pressure, diabetes, high level of cholesterol, tobacco smoking, as well as other vascular risk factors, as pathogenetic cause of AD [6-8]. However, a central role for systemic inflammation has been claimed also taking into account previously reported data, traumatic brain injury and oxidative stress [9-13]. Indeed, only a
Highlights
Editorial Alzheimer’s disease (AD) is a progressive neurological disorder, which represents the most common form of dementia, one of the major causes of disability in later life
Multiple gene-gene and environment interactions cause AD; various risk factors differently act throughout ageing [2,6]
Large data have been collected in the last two decades regarding the putative role of vascular disease, including systemic atherosclerosis, high blood pressure, diabetes, high level of cholesterol, tobacco smoking, as well as other vascular risk factors, as pathogenetic cause of AD [6,7,8]
Summary
Editorial Alzheimer’s disease (AD) is a progressive neurological disorder, which represents the most common form of dementia, one of the major causes of disability in later life. * Correspondence: roberto.monastero@unipa.it 1Department of Experimental Biomedicine and Clinical Neurosciences, University of Palermo, Palermo, Italy Full list of author information is available at the end of the article small percentage of people aged 80 years or over has a pure neurodegenerative AD, and mixed dementia with vascular and/or inflammatory components are present [14]. Acute episodes of systemic inflammation with increased levels of inflammatory mediator tumor necrosis factor-alpha, which are associated with AD [5], have been shown to be associated with long-term cognitive decline in a prospective cohort study of subjects with AD [16].
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