LAUSR

The exact neuropathological mechanism by which the dementia process unfolds is under intense scrutiny. The disease affects about 38 million people worldwide, 70% of which are clinically diagnosed with Alzheimer's disease (AD). If the destruction of synapses essential for learning, planning and decision-making is part of the problem, must the restoration of previously lost synapses be part of the solution? It is plausible that neuronal capacity to restitute information corresponds with the adaptive capacity of its connectivity reserve. A challenge will be to promote the functional connectivity that can compensate for the lost one. This will require better clarification of the remodeling of functional connectivity during the progression of AD dementia and its reversal upon experimental treatment. A major difficulty is to promote the neural pathways that are atrophied in AD dementia while suppressing others that are bolstered. Therapeutic strategies should aim at scaling functional connectivity to a just balance between the atrophic and hypertrophic systems. However, the exact factors that can help reach this objective are still unclear. Similarities between the effects of chronic stress and some neuropathological mechanisms underlying AD dementia support the idea that common components deserve prime attention as therapeutic targets.