Inhibition of Aging in Parkinson's Disease: A Case Study

Dear Editor:

A case of sporadic Parkinson's disease (PD) is described in which conventional treatments were supplemented with several agents that together might resist progression by inhibiting the aging process. These were selected on the basis of their potential ability to aid function in aging mitochondria by maintaining cellular energy resources and resisting oxidative/nitrosative stress.

The patient presented with unilateral hand tremor and a shuffling gait at the age of 60 years. Conventional treatment was withheld at first, but as symptoms progressed, Sinemet MSD, Herts, UK (carbidopa/levodopa) and benzhexol were started, with beneficial results. Three years after the onset of symptoms, nocturnal melatonin was initiated (Puritan's Pride, 0.2–0.8 mg fast release as needed in divided doses), with holidays for 2 nights at the weekend to prevent tolerance (receptor desensitization). Melatonin secretion declines with age, and replacement has the potential to enhance mitochondrial function. ¹

The following year, four years after symptom onset, Lipo-Carn^® (α-lipoic acid plus acetyl-l-carnitine; Healthspan, Guernsey, UK) was added, the aim being to further improve mitochondrial function, potentiate ATP and glutathione synthesis and to reduce toxication processes associated with aging, complex 1 deficiency, and oxidative stress. ² However, symptoms continued to progress, becoming bilateral. These were controlled with the addition of pramipexole and later entacapone, while benzhexol was discontinued.

At six years after onset, symptoms continued to worsen. Therefore, following evidence that high-dose coenzyme Q (CoQ) might slow symptom progression, and with the intention of further enhancing mitochondrial function and electron transport via support of complex I-III activity, ³ and maintaining cortical CoQ, ⁴ CoQ (Puritan's Pride) was added (plus vitamin E), with gradually rising doses to 1200 mg/day.

Eight years from the start of symptoms, the patient reported increased numbers of “better days” with less tremor and shuffling and at the time of writing, 11 years on, there appear to be no somatic symptoms of PD or continued progression. Some residual difficulties with speech remain, however, but there are signs of slow improvement with time.

Previous experience employing CoQ alone in early PD ³ suggests that it may result in some limited slowing of progression, but nevertheless progression continues and there is no improvement of motor functions and no reversal of PD symptoms. By contrast, in the present case, PD symptoms appear to be largely resolved, and progression halted by the combination of melatonin, α-lipoic acid plus acetyl-l-carnitine, and CoQ. Since the natural history of PD is characterized by unremitting progression, this result appears significant.

The patient's current conventional treatment consists of carbidopa/levodopa (750 mg/d), pramipexole (300 mg/d), entacapone (600 mg/d), amitriptyline (25 mg/d), and is supplemented with melatonin (0.2–0.8 mg at night), α-lipoic acid (200 mg/d), acetyl-l-carnitine (250 mg/d), CoQ (maintenance dose 200–400 mg/d), and vitamin E (400 IU/d). Informed consent was given for all supplements.

Further studies are needed with quantitative ratings, but the result suggests that synergies within this combination of antiaging supplements, may have the ability in some cases, in the long term, to lower the risk factor of aging in PD via support of mitochondrial function.