Abstract
Neurogranin (Ng) is a small protein usually expressed in granule-like structures in pyramidal cells of the hippocampus and cortex. However, its clinical value is not fully clear so far. Currently, Ng is proved to be involved in synaptic plasticity, synaptic regeneration, and long-term potentiation mediated by the calcium- and calmodulin-signaling pathways. Due to both the synaptic integrity and function as the growing concerns in the pathogenesis of a wide variety of neurological and mental diseases, a series of researches published focused on the associations between Ng and these kinds of diseases in the past decade. Therefore, in this review, we highlight several diseases, which include, but are not limited to, Alzheimer’s disease, Parkinson disease, Creutzfeldt–Jakob disease, neuro-HIV, neurosyphilis, schizophrenia, depression, traumatic brain injury, and acute ischemic stroke, and summarize the associations between cerebrospinal fluid or blood-derived Ng with these diseases. We propose that Ng is a potential and promising biomarker to improve the diagnosis, prognosis, and severity evaluation of these diseases in the future.
Highlights
Neurogranin (Ng, called RC3, p17, and BICKS) is a protein with a molecular weight of 7.5 kD and composed of 78 amino acids (Watson et al, 1990)
Considerable evidence proves that a synaptic dysfunction is an early event in the pathogenesis of many neurodegenerative diseases, in the Alzheimer’s disease (AD) (DeKosky and Scheff, 1990; Masliah, 2001) and Parkinson disease (PD) (Jellinger, 2012)
Ng has been recommended as a promising biomarker for synapse loss or dysfunction (Brinkmalm et al, 2019)
Summary
Neurogranin (Ng, called RC3, p17, and BICKS) is a protein with a molecular weight of 7.5 kD and composed of 78 amino acids (Watson et al, 1990). Synaptic integrity and function are both the growing concerns in the pathogenesis of a wide variety of neurological and mental diseases (Fyfe, 2015; Hellwig et al, 2015; Yang et al, 2015; Zetterberg and Blennow, 2015; Bereczki et al, 2017; De Vos et al, 2017; Guha et al, 2018; Blennow et al, 2019) In animal experiments, it showed that mice lacking NRGN show a remarkable decline in hippocampus-dependent spatial memory and deficits in hippocampal long-term potentiation (Pak et al, 2000). A cross-sectional and longitudinal observational study of cognitive decline between the symptomatic AD patients and cognitively normal controls proved that the CSF levels of Ng can TABLE 1 | An overview of the major clinical researches involved in Ng published currently
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