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Although direct causal evidence linking plasmalogen depletion to α-synuclein aggregation remains limited, restoration of plasmalogen levels using plasmalogen precursors protects dopaminergic neurons from toxin-induced degeneration in PD models [96], consistent with plasmalogen deficiency contributing to increased dopaminergic vulnerability

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The isolated PH domain of GRK2, named βARK CT based on its historical name, inhibits GRK2-dependent receptor phosphorylation by competing with GRK2 for G βγ [31–33]

It also helps to protect the body from oxidative stress