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Simultaneously, higher S-adenosylmethionine (SAM) availability supports key methylation-dependent pathways, which are crucial for epigenetic regulation and gene expression related to energy metabolism
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This perspective is reinforced by the central gain model of tinnitus, which suggests that tinnitus results from an abnormal compensatory increase in gain (i.e., neural amplification) within the CAS to compensate for a loss of sensory input from the cochlea 9,10,11
In research models, inhibiting NNMT has been associated with preserved SAM and NAD availability, which is the mechanistic basis for studies into cellular energy and substrate handling
doi:10.2215/cjn.0000000700
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