After having experimented occasionally with MPD over decades - long before being diagnosed with so-called "PD" - and now whilst having standard PD symptoms, I encourage the curious PwP to try methylphenidate to see if you get what are sometimes immediate and phenomenally positive effects on energy, mood, strength, mobility. With the usual caveats ...
5 mg is enough in my case for effects that begin in 20 minutes and last 3.5 - 4 hours.
There's a lot of pretty good support for methylphenidate in "PD". Here's one of many studies:
Neuropharmacol. 2008 Dec; 6(4): 379–385.
Neuropharmacological Mechanisms Underlying the Neuroprotective Effects of Methylphenidate
T.J Volz*
Extract (Full article at link):
Abnormal cytoplasmic DA accumulation may also contribute to the development of Parkinson’s disease [5, 22], suggesting the possibility that MPD may be neuroprotective in this disease state as well since MPD treatment has been shown to improve motor function in human Parkinson’s patients [9]. Additionally, MPD provides protection from the behavioral and neurochemical effects of 6-hydroxydopamine in an animal model of Parkinson’s disease [14]. As detailed below, these neuroprotective effects of MPD may be due, at least in part, to its ability to attenuate or prevent abnormal cytoplasmic DA accumulation in dopaminergic neurons by modulating the activity of the DAT and the VMAT-2 through several neuropharmacological mechanisms.
Drugs That Bind to α-Synuclein: Neuroprotective or Neurotoxic?
Joe Kakish 1, Dongsoo Lee 1, Jeremy S Lee 1
Abstract
The misfolding of α-synuclein is a critical event in the death of dopaminergic neurons and the progression of Parkinson's disease. Drugs that bind to α-synuclein and form a loop structure between the N- and C-terminus tend to be neuroprotective, whereas others that cause a more compact structure tend to be neurotoxic. The binding of several natural products and other drugs that are involved in dopamine metabolism were investigated by nanopore analysis and isothermal titration calorimetry. The antinausea drugs, cinnarizine and metoclopramide, do not bind to α-synuclein, whereas amphetamine and the herbicides, paraquat and rotenone, bind tightly and cause α-synuclein to adopt a more compact conformation. The recreational drug, cocaine, binds to α-synuclein, whereas heroin and methadone do not. Metformin, which is prescribed for diabetes and is neuroprotective, binds well without causing α-synuclein to adopt a more compact conformation. Methylphenidate (Ritalin) binds to sites in both the N- and C-terminus and causes α-synuclein to adopt a loop conformation. In contrast, amphetamine only binds to the N-terminus. Except for cinnarizine and metoclopramide, there is a good correlation between the mode of binding to α-synuclein and whether a drug is neuroprotective or neurotoxic.
My approach is still experimental and short term oriented. I take a small dose (5 or 10 mg has been plenty) occasionally to see the effects. No regular dosing and no experience with long-term use. It's been excellent on most tries for getting me up and moving, extending my exercise capacity and abilities, and lifting mood and mental sharpness.
Aside from methylphenidate's potential side effects, and some studies dismissing its usefulness in "PD", here're the downsides in my experience:
1) the effects are variable from one dose to the next. Sometimes even 5 mg will hit me too hard and I'll get a 'stressed-out' reaction. Other times, the same dose will have little effect.
2) can contribute to insomnia.
Do your due-diligence. If you may be a suitable candidate for this drug, I encourage people to give it a try. The effects may be phenomenal.
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