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The supporting evidence is indirect, drawn from studies of endogenous GH pulsatility rather than from a protocol-specific trial [5, 8]

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Elevated LC3-II can arise from impaired fusion of autophagosomes with lysosomes [151], therefore it is possible that both LC3-I and LC3-II levels are increased in PD PBMCs due to disruption of downstream clearance of autophagosomes