Dementia due to Alzheimer's Disease (DAD) is the manly cause of dementia on elderly. Its prevalence increases along with population ageing. Besides, among the most prevalent causes of mortality, DAD is the one without efficient prevention and treatment methods, which makes it a public health issue.The impossibility on preventing and treating DAD is partially due to scarce knowledge about its etiology. Because of this, the study of biomarkers has been one important aspect on recent DAD research.Among laboratory biomarkers, the focus lies in beta-amyloid 42 (betaA42), phosphorylated tau protein (p-tau) and total tau protein (t-tau) on cerebrospinal fluid (CSF). Evidences suggest that betaA42 levels decrease on CSF at amnestic mild cognitive impairment (aMCI) and pre-clinical DAD. It has also been exposed an increase on p-tau and t-tau levels on CSF. However, besides these biomarkers, apolipoprotein E type 4 allele (APOE4) seems to be a risk factor for DAD that may influence on betaA42 deposition at neuritic plaques - which are histopathological evidences of DAD - and their production.Nevertheless, other risk factors are possibly implicated at DAD etiology. Some of them are associated with local and systemic inflammatory response. Thus, DAD is a multifactorial disease with a complex physiopathology. Yet, some studies suggest that oxidative stress and neuroinflammation could be the axis to connect all the other possible pathological mechanisms. Therefore, comprehension of the relationship between inflammatory and neurodegenerative processes is essential to understand physiopathological basis of DAD. Hence, the present study intends to study the relationship between some biomarkers of neuroinflammation (IL-1, IL-6, alfa-TNF, alpha-1 antitrypsin and C-reactive protein) and neurodegeneration biomarkers (betaA42 serum levels, p-tau and t-tau). We expect to obtain data that support hypothesis about DAD physiopathology.
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