Ngrn, also known as neurogranin, seems to be involved in regulating the mitochondrial 16S rRNA and intra-mitochondrial translation as part of a functional module consisting of NGRN, WBSCR16, RPUSD3, RPUSD4, TRUB2, and FASTKD2, which is essential for oxidative phosphorylation [1]. Additionally, it is a potential biomarker in neurodegenerative diseases, especially for synaptic loss in Alzheimer's disease (AD) [2].

In a longitudinal study of patients in the Amsterdam Dementia Cohort, baseline CSF levels of Ngrn in AD patients were higher than in cognitively normal participants, and were highly correlated with total tau and tau phosphorylated at threonine 181, but not with Aβ42. Baseline Ngrn levels were also higher in MCI patients who progressed to AD compared with those with stable MCI, and were predictive of progression from MCI to AD [2]. In another study, when pooling data from GPI and NS patients, plasma Ngrn levels correlated with cognitive scale scores [3].

In conclusion, Ngrn plays a role in regulating mitochondrial translation and is potentially a biomarker for synaptic loss in AD and may be associated with cognitive function in some neurological conditions. These findings from in-vivo-like patient-based studies help understand its biological functions and significance in neurodegenerative diseases.