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This theory assumes that AD is due to the cellular deposition of insoluble amyloid (A) protein fragments arising from amyloid precursor protein proteolysis

DSIP has been described as influencing GABA-A receptor activity in a way sometimes compared to benzodiazepines but, importantly, without the sedation or dependence profile associated with those drugs

The clinical record must clearly demonstrate the providers active oversight and the medical necessity of the prolonged treatment

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