Targeting and increasing the expression ofNlgn1 to promote its neuroprotective effects at synapsesoffers a therapeutic opportunity in slowing down neurodegenerativeprocesses.62,73 A different study demonstrated reduced MeCP2 levels inthe striatum of 3-month-old APP/PS1 mice compared to controls, with specificS421 phosphorylation of MeCP2 shown to be increased in the cytoplasm in neurons.The authors suggested that this finding was due to de novo phosphorylation ofMeCP2 after AD pathological injury, possibly acting to relieve transcriptionalrepression.63 The gene discussed is APP; the disease is Alzheimer disease.