TNF and Parkinson disease: Patient monocytes may be compromised by the effects of PD drug regimens and the patients’ physiological status, whereas pMac have never been exposed to patient cytokines, drugs, etc. Consistent with this, pMac do not produce TNFα in response to monomeric or fibrillar αS or SNCA mutation, presumably because they have not been exposed to any priming cytokines, whereas increased TNFα shown to be released from mouse microglia overexpressing SNCA is likely due to chronic activation in the in vivo system23, 24.