Objective: We aimed to investigate the changes in SN echogenicity in primate models of hemiparkinsonism induced by 6-OHDA.

Background: Hyperechogenicity in the midbrain demonstrated by transcranial sonography (TCS) is reported to be a marker of Parkinson’s disease (PD). The mechanism of hyperechogenicity in the SN is unknown but it is assumed to be related to the increased amount of iron in the SN, supported by postmortem and animal studies.

Method: 6 male Sapajus apella monkeys, aged between 18 and 26 years of age, were separated in three groups: Control (n=2), 6-OHDA-induced hemiparkinsonism (n=4), and sham-operated animals (n=2). Control subjects were left undisturbed, while 6-OHDA and SHAM were submitted to stereotaxic neurosurgery for microinjections of 6-OHDA or saline (sham) in 12 sites on the substantia nigra and striatum. After recovery, the animals were evaluated with a modified version of the UPDRS adapted for primates and underwent motor tasks to confirm the establishment of hemiparkinsonism. Before the intervention and twelve weeks after the establishment of hemiparkinsonism, all subjects were submitted to TCS for detection of changes in SN echogenicity.

Results: We observed no differences in the mesencephalic areas (1,82±0,6cm² before / 1,47±0,44 cm² after), and no hyperechogenic pattern was detected in the SN of the subjects, for all groups. Immunohistochemistry for tyrosine hydroxylase positive neurons showed great reduction of TH+ neurons on the SN injected side in 6-OHDA group.

Conclusion: The mechanisms behind the SN hyperechogenicity observed in PD patients seem to not be related to neural loss induced by 6-OHDA in PD primate models.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/hemiparkinsonism-induction-with-6-ohda-in-primates-does-not-induce-sn-hyperechogenicity/