Acetylcholinesterase (AChE) hydrolyzes ACh into choline and acetate, thereby terminating neurotransmission and preventing continuous nerve impulses at nerve terminals, making it a prime therapeutic target for diseases that occur with a cholinergic deficit, prominently Alzheimer’s disease (AD) and myasthenia gravis (MG) [4,5]. Here, ACHE is linked to early-onset autosomal dominant Alzheimer disease.