The protective effects of nicotinamide and PARP-1 inhibition on oxidative death, mitochondrial dysfunction and microglial activation, in addition to the well-known beneficial effect of increasing NAD+ pools support the idea that nicotinamide and other PARP-1 inhibitors constitute a new pathway to find molecular targets for the treatment of early stages of AD (Figure 1). Here, PARP1 is linked to Alzheimer disease.