We hypothesize that accumulation of these complexes might result in pathology due to the formation of misfolded GCAP2 oligomers, in much a similar way to which synuclein, APP, Tau, Huntingtin or ataxin lead to neuronal cell death in Parkinson's (PD), Alzheimer (AD), Huntington's (HD) or spinocerebellar ataxia (SCA) diseases. The gene discussed is GUCA1B; the disease is Alzheimer disease.