Experimental inhibition or genetic knockdown of PARP-1 has been shown to reduce Aβ42 isoform plaques and consequently reestablish locomotor activity in transgenic Drosophila models of AD; in addition to a great increase in nicotinamide adenine dinucleotide (NAD+, of which depletion is a well-known and important hallmark of neurodegeneration) levels in the brain of studied flies; a strong decrease in DNA transposable elements, which are known to be excessively transcribed in many NDDs, including AD and PD; and an amelioration of life expectancy [109]. Here, PARP1 is linked to Alzheimer disease.