Abstract
Neurodegenerative diseases are a burden of our century. Although significant efforts were made to find a cure or relief to this scourge, their pathophysiology remains vague and the cellular function of the key involved proteins is still unclear. However, in the case of amyloid β (Aβ), a key protein concerned in Alzheimer disease, we are now a step closer in the unscrambling of its cellular functions. Interestingly, whereas the exact role of Aβ in the pathophysiology of Alzheimer disease is still unresolved, a recent study revealed a neuroprotective function of Aβ in multiple sclerosis with possibly promising therapeutic benefits.