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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.