12 / 21
Page 42
December 06-07 , 2018
Amsterdam, Nether l ands
Journal of Neuropsychiatry
ISSN: 2471-8548
Alzheimer’s and Dementia 2018
1 3
t h
W o r l d c o n g r e s s o n
Alzheimer’s and Dementia
P
ET 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 (Pittsburgh Compound B) 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 were seen in non-memory functions.
Most importantly, the absence of amyloid in mild cognitive impairment (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 neuro-degeneration, 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.
Panteleimon.Giannakopoulos@unige.chAmyloid deposition in brain aging: causal agent or
innocuous by stander ?
P Giannakopoulos, C Rodriguez and S Haller
1
University of Geneva, Switzerland
2
University Hospitals of Geneva, Switzerland
3
Uppsala University, Sweden
gA dea Carouge Radiologic Diagnostic Center, Geneva, Switzerland
J Neurol Neurosci 2018, Volume: 2
DOI: 10.21767/2471-8548-C1-003