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Members of the Department of Biochemistry and Molecular Genetics




                  a limited precision of these assays in early phases, highlight the need
                  to identify new markers, in particular in more accessible biological
                  fluids such as blood. Currently, many researchers believe that both
                  the development of neurofibrillary and amyloid pathologies in AD
                  represent relatively late events in the evolution of the disease, which
                  may or may not reflect the fundamental biochemical-molecular dys-
                  functions that give rise to the disease. The clinical manifestations of
                  AD are preceded by an asymptomatic preclinical phase, after which
                  the first symptoms appear in the prodromal phase of the disease
                  characterized by mild cognitive impairment (MCI). In this sense, AD
                  can be understood as a continuous process that evolves from the
                  asymptomatic phases to the dementia phase. This evolution is largely
                  determined by genetic risk variants and is associated with biochemi-
                  cal changes that can ideally serve as early markers of the disease.
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