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RESEARCH PRODUCT
Alzheimer’s disease and infections, where we stand and where we go
Sonya VastoCalogero CarusoRoberto Monasterosubject
AgingTraumatic brain injuryImmunologyTau proteinperiodontal diseaseDiseaseInfectionsBioinformaticsAtrophyAlzheimer'MedicineDementiaRisk factorAlzheimer's; infections; herpes viruses; periodontal disease; infectionInflammationSettore MED/04 - Patologia Generalebiologybusiness.industryVascular diseaseHerpes virusesOdds ratiomedicine.diseaseinfectionAgeingEditorialImmunologybiology.proteinherpes viruseSettore MED/26 - NeurologiabusinessAlzheimer’s diseasedescription
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
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2014-12-01 | Immunity & Ageing |