Loss of functional mitochondrial complex I (MCI) in the dopaminergic neurons of the substantia
nigra is a hallmark of Parkinson’s disease 1 . Yet, whether this change contributes to …

Mitochondrial and lysosomal dysfunction have been implicated in substantia nigra dopaminergic
neurodegeneration in Parkinson’s disease (PD), but how these pathways are linked in …

Calcium handling by mitochondria is a key feature in cell life. It is involved in energy production
for cell activity, in buffering and shaping cytosolic calcium rises and also in determining …

Presenilin mutations are the main cause of familial Alzheimer's disease (FAD). Presenilins
also play a key role in Ca 2+ homeostasis, and their FAD-linked mutants affect cellular Ca 2+ …

Parkinson's disease (PD) is the second most common neurodegenerative disease in the
world. Its causes are poorly understood and there is no proven therapeutic strategy for slowing …

How do neurons match generation of adenosine triphosphate by mitochondria to the bioenergetic
demands of regenerative activity? Although the subject of speculation, this coupling is …

Monoamine oxidase (MAO) metabolizes cytosolic dopamine (DA), thereby limiting auto-oxidation,
but is also thought to generate cytosolic hydrogen peroxide (H 2 O 2 ). We show that …

Mutations in amyloid precursor protein (APP), and presenilin‐1 and presenilin‐2 (PS1 and
PS2) have causally been implicated in Familial Alzheimer’s Disease (FAD), but the …

Degeneration of substantia nigra (SN) dopaminergic (DAergic) neurons is responsible for
the core motor deficits of Parkinson’s disease (PD). These neurons are autonomous …

We have previously shown that familial Alzheimer’s disease mutants of presenilin‐2 (PS2)
and, to a lesser extent, of presenilin‐1 (PS1) lower the Ca 2+ concentration of intracellular …