Peripheral determination of iPLA2 enzyme activity and evaluation of functional markers of the blood-brain barrier in patients with Alzheimer's Disease

• Grant number: 18/08111-0
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: December 01, 2018
• End date: November 30, 2019
• Field of knowledge: Health Sciences - Medicine - Psychiatry
• Principal Investigator: Wagner Farid Gattaz
• Grantee: Vitor Macedo Brito Medeiros
• Host Institution: Instituto de Psiquiatria Doutor Antonio Carlos Pacheco e Silva (IPq). Hospital das Clínicas da Faculdade de Medicina da USP (HCFMUSP). Secretaria da Saúde (São Paulo - Estado). São Paulo , SP, Brazil

Abstract

In view of the socio-demographic challenges imposed and the high functional impact of Alzheimer's disease (AD), it is important to carry out studies that aim to uncover the pathophysiological mechanisms underlying this disease. Such understanding will broaden the spectrum of substrates with potential use as biomarkers, thus contributing to early diagnoses, as well to discover pathological pathways and thus novel pharmacological targets. Therefore, studies are emerging that seek to relate findings consolidated in the literature, looking forward to understand how the pathology of AD develops. The relationship of AD with the integrity of the blood-brain barrier (BBB) stands out among the characteristics of the disease that still require elucidation. It is known that in AD this structure is dysfunctional. Such an event can be related to lymphocytic infiltration in the brain and the installation of an inflammatory process described as key to establish the disease. Based on this assumption, this project proposes that a potential justification for this effect may be related to the already remarkable decrease in activity of the enzyme iPLA2 in patients with AD, and consequent reduced availability of its products. The aim of this study is to evaluate the correlation between the rupture of the blood-brain barrier, quantified by the Q-albumin test, and the activity of iPLA2 in patients with AD.