There has been much concern that levodopa hastens the progression of PD. Many studies have found this not to be the case. Now Japanese researchers have found that in a mouse model:
"results suggest that L-DOPA may slow the progression of PD in vivo by suppressing the aggregation of α-synuclein in dopaminergic neurons and the cell-to-cell propagation of abnormal α-synuclein. This is the first report describing the suppressing effect of L-DOPA/benserazide on the propagation of pathological α-synuclein".
Early days!
Reference:
Front Neurosci. 2019; 13: 595.
Published online 2019 Jun 14. doi: 10.3389/fnins.2019.00595
PMCID: PMC6587610
PMID: 31258461
Effect of L-DOPA/Benserazide on Propagation of Pathological α-Synuclein
Aki Shimozawa,1,2 Yuuki Fujita,1,2 Hiromi Kondo,1 Yu Takimoto,3 Makoto Terada,1 Masanao Sanagi,3 Shin-ichi Hisanaga,2 and Masato Hasegawa1,*
"In an open-label pilot study, in patients with newly diagnosed nAMD and naïve to anti-VEGF injections (Cohort-1), the effects of carbidopa-levodopa on vision and anatomic outcomes were evaluated for 4 weeks. Then patients were followed 5 months further with ascending levodopa doses. Patients previously treated with anti-VEGF injection therapy (Cohort-2) were also treated with ascending levodopa doses and evaluated for 6 months.
Results
Levodopa was safe, well tolerated, and delayed anti-VEGF injection therapy while improving visual outcomes. In the first month, retinal fluid decreased by 29% (P = .02, n = 12) without anti-VEGF treatment. Through 6 months the decrease in retinal fluid was sustained, with a mean frequency of 0.38 injections/month. At month 6, mean visual acuity improved by 4.7 letters in Cohort-1 (P = .004, n = 15) and by 4.8 letters in Cohort-2 (P = .02, n = 11). Additionally, there was a 52% reduction in the need for anti-VEGF injections in Cohort-2 (P = .002)."
Risk factors for progression of age-related macular degeneration
" A recent epidemiologic study showed that patients with PD treated with levodopa less often developed AMD (OR 0.78) and at a later age (mean age of onset 79 years) compared to untreated patients (mean age of onset 71 years).164 Levodopa is shown to stimulate the GRP143 receptor which decreases the release of VEGF and exosomes with inflammatory factors from RPE cells.165 Currently, clinical trials are investigating whether treatment with levodopa may indeed reduce the inflammatory reaction of the retina and slow down disease progression in AMD. Although it is not likely that PD and AMD are directly associated, both neurodegenerative diseases share probably some underlying pathophysiological features."
" Levodopa was used as a treatment of amblyopia alone or in combination with classical treatment of occlusion. Visual acuity is improved after treatment with oral Levodopa. When is used as an adjunct to the occlusion therapy, Levodopa can be associated with long-term improvement in the vision, and may have also better compliance for patching. Levodopa stimulates the brain plasticity in adult age and can be used in treatment for amblyopia. Patients have also an increase of the visual acuity after orthoptic treatment for amblyopia and when Levodopa is administered, the vision increases much more. Contrary to the classical conception, according to which amblyopia cannot be treated after 10-12 years of age and it is untreatable in adults, studies about treatment with Levodopa in amblyopic eyes, may allow the improvement of the visual acuity in adults, as well"
Mouse model findings rarely replicate in humans. Major human studies find that early suspicion of benefit from levodopa did NOT replicate when allowing a sufficient period for levodopa washout. Here's an easy to read summary. journals.lww.com/neurotoday...
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