We have shown that near infrared light (NIr), directed transcranially, mitigates the loss of midbrain dopaminergic cells in MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine)-treated mice, a well-established model of Parkinson’s disease. These findings add to a body of work suggesting NIr treatment protects against, or accelerates recovery from, damage by various different insults.

However one puzzling feature of NIr treatment is the reported lack of laterality in tissue response. For example, in soft tissue injury, the response is typically bilateral despite only unilateral exposure. We hypothesise therefore that NIr-induced neuroprotection may be partly indirect, possibly mediated by circulating ‘factors’.

To test this hypothesis, we applied NIr to the dorsum of MPTP-treated mice, shielding the head from radiation using a ‘helmet’ of impenetrable foil. Dopaminergic cell number in the substantia nigra pars compacta was determined by tyrosine hydroxylase (TH) labelling, and compared to measures in MPTP-treated mice receiving NIr directed at the head (but in practice reaching the whole dorsum), as well untreated MPTP- and saline-injected controls (n=10/group).

Despite receiving no direct irradiation of the skull, MPTP-treated mice receiving NIr to the dorsum had significantly higher (20%) TH⁺ cell number than non-irradiated MPTP-treated mice (p<0.05). However protection was not complete, with 15% fewer TH⁺ cells than saline-treated controls (p<0.05). MPTP-treated mice receiving NIr to the head showed no significant decline in TH⁺ cell number relative to saline-treated controls (p>0.05).

The findings suggest NIr-induced neuroprotection may be mediated partly, but not entirely, by a systemic or indirect effect. Flow cytometry experiments are currently underway to determine the nature of any immune system involvement.