Research articles on Antiparkinson agents:
The evolution of use of anti-Parkinson drugs in Spain.
Working hypothesis for the effect of GABAergic, glycinergic or glutamatergic drugs in the treatment of Parkinson disease.
Motor function in the normal aging population: treatment with levodopa.
Pramipexole vs levodopa as initial treatment for Parkinson disease: A randomized controlled trial. Parkinson Study Group.
  SELEGILINE (brand names: Carbex, Jumex, Eldepryl)  

Eldepryl is prescribed along with Carbidopa) for people with Parkinson's disease. It is used when Sinemet no longer seems to be working well. Eldepryl has no effect when taken by itself; it works only in combination with Larodopa (levodopa) or Sinemet. Parkinson's disease, which causes muscle rigidity and difficulty with walking and talking, involves the progressive degeneration of a particular type of nerve cell. Early on, Larodopa or Sinemet alone may alleviate the symptoms of the disease. In time, however, these medications work less well; their effectiveness seems to switch on and off at random, and the individual may begin to experience side effects such as involuntary movements and "freezing" in mid-motion. Eldepryl may be prescribed at this stage of the disease to help restore the effectiveness of Larodopa or Sinemet. When you begin to take Eldepryl, you may need a reduced dosage of the other medication.

You can find an extensive list of recent scientific research abstracts about Selegiline here


Caution! Before starting to take this medicine, it is vital that you should consult your doctor! Do not use it on your own initiative, without medical advice.

You can find an extensive list of recent scientific research abstracts about LEVODOPA-MADOPAR 250 MG here


Sinemet CR is a controlled-release tablet that may be given to help relieve the muscle stiffness, tremor, and weakness caused by Parkinson's disease. It may also be given to relieve Parkinson-like symptoms caused by encephalitis (brain fever), carbon monoxide poisoning, or manganese poisoning. Sinemet CR contains two drugs, Carbidopa and levodopa. The drug that actually produces the anti-Parkinson's effect is levodopa. Carbidopa prevents vitamin B6 from destroying levodopa, thus allowing levodopa to work more efficiently. Parkinson's drugs such as Sinemet CR relieve the symptoms of the disease, but are not a permanent cure.

You can find an extensive list of recent scientific research abstracts about LEVODOPA-SINEMET here

  MIRAPEX (MIRAPEXIN) (brand name: Mirapex)  

Although it is not a cure, Mirapex eases the symptoms of Parkinson's disease - a progressive disorder marked by muscle rigidity, weakness, shaking, tremor, and eventually difficulty with walking and talking. Parkinson's disease results from a shortage of the chemical messenger dopamine in certain areas of the brain. Mirapex is believed to work by boosting the action of whatever dopamine is available. The drug can be used with other Parkinson's medications such as Eldepryl, Sinemet, and Larodopa

You can find an extensive list of recent scientific research abstracts about MIRAPEX (MIRAPEXIN) here


Rev Neurol. 2002 Apr 1-15;34(7):612-7
The evolution of use of anti-Parkinson drugs in Spain.
Montane E, Vallano Ferraz A, Castel JM.
Servicio de Farmacologia Clinica, Hospital Universitario Vall d'Hebron, Barcelona, Espana.

INTRODUCTION. In recent years new anti Parkinson drugs have been marketed and there has been controversy over the safety of some drugs. OBJECTIVE. To analyze the evolution of the consumption of anti Parkinson drugs and the effect of the newer drugs. PATIENTS AND METHODS. A study of the consumption of anti Parkinson drugs (1989 1998). Data were obtained from the ECOM database of the Ministry of Health and TEMPUS of the National Statistics Institute. The drugs were classified using the Anatomo Therapeutic Clinical Classification (ATC). Consumption was expressed in defined daily dosage (DDD) and the costs in euros. The drugs marketed since 1990 were classified as new drugs and the others as classical drugs. RESULTS. The total consumption of drugs increased from 1.92 DDD/1,000 inhabitants/day in 1989 to 3.64 DDD/1,000 inhabitants/day in 1998. The drugs showing the greatest increase were selegiline, pergolide and levodopa. The total pharmaceutical expenses tripled. There was a smaller increase in the consumption of new drugs (1.2% of the total in 1991 and 6.6% in 1998) than in their costs (6.7% of the total in 1991 and 38.8% in 1998). The cost per DDD of the new drugs increased five times (1989: 2.55 euros and 1998: 13.59 euros) and that of the classical drugs was similar (1989: 0.54 euros and 1998: 0.62 euros). CONCLUSIONS. The total consumption of anti Parkinson drugs has progressively increased. The consumption of selegiline has also increased in spite of controversy over its safety. The new drugs have a major economic effect.


Ann Pharm Fr. 1990;48(2):70-80
Working hypothesis for the effect of GABAergic, glycinergic or glutamatergic drugs in the treatment of Parkinson disease.
Vamvakides A.
Laboratoire Chropi, Paris.

The data obtained during the past decade in experimental and clinical pharmacology show that the GABAergic drugs, with central activity, do not ameliorate the symptoms of the Parkinson's disease (PD), but would worsen the akineto-rigid syndrome, the dyskinesias and the deteriorating mental status in the later stages of the PD. On the other hand, recent data of experimental pharmacology suggest the possibility that glycinergic or glutamatergic derivatives, with central activity, would have a beneficial effect on the syndromes of the later stages of PD (declining efficacy of L-DOPA, dyskinesias, deteriorating mental status), which constitute, with the fluctuation of the response to L-DOPA, ("on-off" effects), the major problems of the PD's treatment. Some theoretical and experimental data also suggest the possibility of a beneficial effect of the glutamatergic drugs in the treatment of the "on-off" effects.



Neurology 1985 Apr;35(4):571-3
Motor function in the normal aging population: treatment with levodopa.
Newman RP, LeWitt PA, Jaffe M, Calne DB, Larsen TA.

In normal elderly humans there is progressive motor dysfunction and loss of nigrostriatal neurons and brain dopamine similar to, although of a milder degree than, that seen in Parkinson's disease. Ten healthy elderly volunteers were given Carbidopa/levodopa or placebo in a double-blind crossover study. We measured movement velocity, reaction time, tremor, visual evoked response (VER), and electroretinography (ERG). Significant changes were seen only in ERG. Motor functions and VER were unchanged. Although there appeared to be pharmacologic activity (ie, changes in ERG), levodopa, in adequate antiparkinson dosage, had no impact on the mild extrapyramidal impairment of normal elderly subjects.



JAMA 2000 Oct 18;284(15):1931-8
Pramipexole vs levodopa as initial treatment for Parkinson disease: A randomized controlled trial. Parkinson Study Group.
Parkinson Study Group.

CONTEXT: Pramipexole and levodopa both ameliorate the motor symptoms of early Parkinson disease (PD), but no controlled studies have compared long-term outcomes after initiating dopaminergic therapy with pramipexole vs levodopa. OBJECTIVE: To compare the development of dopaminergic motor complications after initial treatment of early PD with pramipexole vs levodopa. DESIGN: Multicenter, parallel-group, double-blind, randomized controlled trial. SETTING: Academic movement disorders clinics at 22 sites in the United States and Canada. PATIENTS: Three hundred one patients with early PD who required dopaminergic therapy to treat emerging disability, enrolled between October 1996 and August 1997. INTERVENTIONS: Subjects were randomly assigned to receive pramipexole, 0.5 mg 3 times per day, with levodopa placebo (n = 151); or Carbidopa/levodopa, 25/100 mg 3 times per day, with pramipexole placebo (n = 150). For patients with residual disability, the dosage was escalated during the first 10 weeks. From week 11 to month 23.5, investigators were permitted to add open-label levodopa to treat continuing or emerging disability. MAIN OUTCOME MEASURES: Time to the first occurrence of any of 3 dopaminergic complications: wearing off, dyskinesias, or on-off motor fluctuations; changes in scores on the Unified Parkinson's Disease Rating Scale (UPDRS), assessed at baseline and follow-up evaluations; and, in a subgroup of 82 subjects evaluated at baseline and 23.5 months, ratio of specific to nondisplaceable striatal iodine 123 2-beta-carboxymethoxy-3-beta-(4-iodophenyl)tropane (beta-CIT) uptake on single photon emission computed tomography imaging of the dopamine transporter. RESULTS: Initial pramipexole treatment resulted in significantly less development of wearing off, dyskinesias, or on-off motor fluctuations (28%) compared with levodopa (51%) (hazard ratio, 0.45; 95% confidence interval [CI], 0. 30-0.66; P<.001). The mean improvement in total UPDRS score from baseline to 23.5 months was greater in the levodopa group than in the pramipexole group (9.2 vs 4.5 points; P<.001). Somnolence was more common in pramipexole-treated patients than in levodopa-treated patients (32.4% vs 17.3%; P =.003), and the difference was seen during the escalation phase of treatment. In the subgroup study, patients treated initially with pramipexole (n = 39) showed a mean (SD) decline of 20.0% (14.2%) in striatal beta-CIT uptake compared with a 24.8% (14.4%) decline in subjects treated initially with levodopa (n = 39; P =.15). CONCLUSIONS: Fewer patients receiving initial treatment for PD with pramipexole developed dopaminergic motor complications than with levodopa therapy. Despite supplementation with open-label levodopa in both groups, the levodopa-treated group had a greater improvement in total UPDRS compared with the pramipexole group.


on the Adriatic Coast
The Anti-Aging Fasting Program consists of a 7-28 days program (including 3 - 14 fasting days). 7-28-day low-calorie diet program is also available .
More information
    The anti-aging story (summary)
Introduction. Statistical review. Your personal aging curve
  Aging and Anti-aging. Why do we age?
    2.1  Aging forces (forces that cause aging
Internal (free radicals, glycosylation, chelation etc.) 
External (Unhealthy diet, lifestyle, wrong habits, environmental pollution, stress, poverty-change "poverty zones", or take it easy. etc.) 
    2.2 Anti-aging forces
Internal (apoptosis, boosting your immune system, DNA repair, longevity genes) 
External (wellness, changing your environment; achieving comfortable social atmosphere in your life, regular intake of anti-aging drugs, use of replacement organs, high-tech medicine, exercise)
    2.3 Aging versus anti-aging: how to tip the balance in your favour!
    3.1 Caloric restriction and fasting extend lifespan and decrease all-cause mortality (Evidence)
      Human studies
Monkey studies
Mouse and rat studies
Other animal studies
    3.2 Fasting and caloric restriction prevent and cure diseases (Evidence)
Hypertension and Stroke
Skin disorders
Mental disorders
Neurogical disorders
Asthmatic bronchitis, Bronchial asthma
Bones (osteoporosis) and fasting
Arteriosclerosis and Heart Disease
Cancer and caloric restriction
Cancer and fasting - a matter of controversy
Eye diseases
Chronic fatigue syndrome
Sleeping disorders
Rheumatoid arthritis
Gastrointestinal diseases
    3.3 Fasting and caloric restriction produce various
      biological effects. Effects on:
        Energy metabolism
Lipids metabolism
Protein metabolism and protein quality
Neuroendocrine and hormonal system
Immune system
Physiological functions
Reproductive function
Cognitive and behavioral functions
Biomarkers of aging
    3.4 Mechanisms: how does calorie restriction retard aging and boost health?
        Diminishing of aging forces
  Lowering of the rate of gene damage
  Reduction of free-radical production
  Reduction of metabolic rate (i.e. rate of aging)
  Lowering of body temperature
  Lowering of protein glycation
Increase of anti-aging forces
  Enhancement of gene reparation
  Enhancement of free radical neutralisation
  Enhancement of protein turnover (protein regeneration)
  Enhancement of immune response
  Activation of mono-oxygenase systems
  Enhance elimination of damaged cells
  Optimisation of neuroendocrine functions
    3.5 Practical implementation: your anti-aging dieting
        Fasting period.
Re-feeding period.
Safety of fasting and low-calorie dieting. Precautions.
      3.6 What can help you make the transition to the low-calorie life style?
        Social, psychological and religious support - crucial factors for a successful transition.
Drugs to ease the transition to caloric restriction and to overcome food cravings (use of adaptogenic herbs)
Food composition
Finding the right physician
    3.7Fasting centers and fasting programs.
  Food to eat. Dishes and menus.
    What to eat on non-fasting days. Dishes and menus. Healthy nutrition. Relation between foodstuffs and diseases. Functional foods. Glycemic index. Diet plan: practical summary. "Dr. Atkins", "Hollywood" and other fad diets versus medical science

Bread, cereals, pasta, fiber
Glycemic index
Meat and poultry
Sugar and sweet
Fats and oils
Dairy and eggs
Nuts and seeds
Food composition

  Anti-aging drugs and supplements
    5.1 Drugs that are highly recommended
      (for inclusion in your supplementation anti-aging program)
        Vitamin E
Vitamin C
Co-enzyme Q10
Lipoic acid
Folic acid
Flavonoids, carotenes
Vitamin B
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Muscle weakness
Parkinson's disease
Prostate hyperplasia
Sexual disorders
Stroke risk
Weight gaining
    5.4 The place of anti-aging drugs in the whole
      program - a realistic evaluation
    6.1 Early diagnosis of disease - key factor to successful treatment.
      Alzheimer's disease and Dementia
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Parkinson's disease
Prostate hyperplasia
Stroke risk
Weight gaining
    6.2 Biomarkers of aging and specific diseases
    6.3 Stem cell therapy and therapeutic cloning
    6.4 Gene manipulation
    6.5 Prosthetic body-parts, artificial organs
Bones, limbs, joints etc.
Heart & heart devices
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Weight-lifting - body-building
Professional sport: negative aspects
  Conclusion: the whole anti-aging program
    9.1 Modifying your personal aging curve
      Average life span increment. Expert evaluation.
Periodic fasting and caloric restriction can add 40 - 50 years to your lifespan
Regular intake of anti-aging drugs can add 20-30 years to your lifespan
Good nutrition (well balanced, healthy food, individually tailord diet) can add 15-25 years to your lifespan
High-tech bio-medicine service can add 15-25 years to your lifespan
Quality of life (prosperity, relaxation, regular vocations) can add 15-25 years to your lifespan
Regular exercise and moderate physical activity can add 10-20 years to your lifespan
These approaches taken together can add 60-80 years to your lifespan, if you start young (say at age 20). But even if you only start later (say at 45-50), you can still gain 30-40 years

Click image
to view
    9.2 The whole anti-aging life style - brief summary 
    References eXTReMe Tracker
        The whole anti-aging program: overview

Home Contact Us ANTI-AGING GUIDE 2003