Panteleimon Giannakopoulos
University Hospitals of Geneva, Switzerland
Title: Amyloid deposition in brain aging: Causal agent or innocuous bystander?
Biography
Biography: Panteleimon Giannakopoulos
Abstract
PET amyloid imaging has been initially considered as the main tool to investigate the beginning of the AD process in cognitively intact individuals. The percentage of PET-amyloid positive controls is of 6% at age 60 but reaches 50% at age 90 in community-based sample pointing to the fact that amyloid deposition (as amyloid plaque formation) is closely related to aging process. In fact, increased PiB binding has been reported in almost 20%-30% of cognitively preserved elders mainly in posterior cingulate cortex, precuneus and prefrontal cortex. Compared with amyloid-negative, amyloid-positive controls showed moderate decline in verbal and visual episodic memory over 36 months but no changes in non-memory functions. Most importantly, the absence of amyloid in MCI cases is associated with cognitive stability at 36 months. Increased PET-PiB binding is associated with brain atrophy, cortical thinning but also decreased cortical metabolism, aberrant functional connectivity at rest and decreased task-related deactivation of the default mode network. Altogether these data suggest that contrasting with CSF Aß and tau changes that sign a biological diathesis to neurodegeneration, amyloid positivity in the human brain is present as a part of the aging process representing a critical step preceding the installation of AD pathophysiology. However, not all cases with elevated PET-PiB bindings evolve to AD and several cases develop dementia not necessarily related to amyloid aggregation.Several recent contributions revealed that neurodegeneration takes place without a temporal link with fibrillar amyloid deposits. Alternative but less frequent pathways exist starting from tau deposition with modest Aß pathology.