AKAP1 and neurodegenerative disease: Altogether, our data support a model of NLPD-PKA in which RIβL50R forms highly partitioned gel-like condensates that can retain substantially more Cα than RIβWT condensates (Figures 5I, 5K, and 5L), dysregulating PKA activity both globally and at AKAP signaling microdomains, leading to several hallmarks of neurodegenerative disease including apoptotic cell death and decreased neurite outgrowth (Figure 6).