Genetic studies have provided clarity on the causative mutations in familial forms of Alzheimer’s disease, where characterized variants in the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes have been shown to be nearly but not fully penetrant [26], whereas familial Parkinson’s mutations in genes like leucine-rich repeat kinase 2 (LRRK2), glucocerebrosidase (GBA), Parkin (PRKN), and alpha-synuclein (SCNA) have been useful for determining PD risk, diagnosis, and disease progression [27]. This evidence concerns the gene PRKN and early-onset autosomal dominant Alzheimer disease.