The “cell cycle hypothesis” for neurodegenerative diseases suggests a link between "cell cycle-like reactivation" and neuronal death, mainly in Alzheimer disease (AD), one of the most common neurodegenerative diseases for which an efficient treatment is yet to be identified. The “insult” represented by Aβ deposits, a typical hallmark of AD, could force the neuron to re-enter the cell cycle. However, a highly differentiated cell unable to successfully accomplish a task normally attributable to immature cells, would end up in neuronal death. Considering neurodegeneration as a result of the abnormal activation in mature cells of a pathway that is typical of immature cells, the results shown in this book propose CLIC1 as part of this pathway, physiological and “successful” in immature cells, contributing to mantain growth cone morphology and sustaining axon outgrowth modulated by cAMP via PKA, but leading to cell death in “mature” neurons. Increased CLIC1 expression in the gangliar layer in AD mouse models before cognitive symptoms, proposes it as an early marker of AD. This study suggests a double role of CLIC1, in retinal ganglion cells physiology and pathology.