டவுன் சிண்ட்ரோம் & குரோமோசோம் அசாதாரணங்களின் ஜர்னல்
திறந்த அணுகல்
ஐ.எஸ்.எஸ்.என்: 2472-1115
ஐ.எஸ்.எஸ்.என்: 2472-1115
Federico Licastro and Elisa Porcellini
Alzheimer’s disease (AD) is a neurodegenerative brain alteration and a leading cause of cognitive decline and dementia and incidence and prevalence of AD are increasing in both industrial and rural societies. However, in spite of intensive research during last thirty years no effective medication is available. Neuropathological AD hallmarks are amyloid deposition and neurofibrillary tangles, however, presence of these brian deposits do not completely explain the disease’s pathogenesis. Recently Aβ peptide, the proteinaceous precursor of brain amyloid deposits, has been proposed as an anti-microbial factor. Recent investigations have indeed shown that virus and/or bacterial infections influenced the clinical history of AD. Genotypic, phenotypic, epidemiological and clinical variables have been associated with an increased risk of cognitive decline or dementia as assesed by longitudinal population investigations. For instance, our data suggested that some genetic signatures, as shown by the AD genome wide association studies, might decrease host antimicrobial immune responses and affect progression to clinical dementia in the elderly by increasing susceptibility to herpes virus infections. The aim of this commentary is to briefly show innovative applicative procedures to determine individual risk of dementia and the possibility to modulate cognitive decline/dementia risk by personalized preventive interventions. The approach presented here may have clinical relevance in adult people with Down’s syndrome that are considered at elevated risk of developing cognitive decline and senile dementia after their 50’ths of age.