For example, in different animal models of Alzheimer’s disease, A2AR are upregulated and A2AR blockade is associated with an increase (recovery) of hippocampal LTP and amelioration of memory deficits [54, 55], whereas A2AR blockade in control animals decreases LTP magnitude without affecting memory performance [54, 55]. The gene discussed is ADORA2A; the disease is early-onset autosomal dominant Alzheimer disease.