6.1 Parkinson's disease 
Early diagnosis of orthostatic hypotension in idopathic Parkinson's disease.
Methods for the early diagnosis of Parkinson's disease.
Plasma measurement of D-dimer levels for the early diagnosis of ischemic stroke subtypes.
Loss of olfaction in de novo and treated Parkinson's disease: possible implications for early diagnosis.
Early diagnosis of Parkinson's disease.
The early diagnosis of Parkinson's disease.
Early differential diagnosis of Parkinson's disease with 18F-fluorodeoxyglucose and positron emission tomography.
PET studies on the early and differential diagnosis of Parkinson's disease.
Catechol metabolites in the cerebrospinal fluid as possible markers in the early diagnosis of Parkinson's disease.
Effect of early diagnosis and therapy on prognosis of Parkinson syndrome.
Folia Med Cracov. 2002;43(1-2):59-67.
Early diagnosis of orthostatic hypotension in idopathic Parkinson's disease
Krygowska-Wajs A, Furgala A, Laskiewicz J, Szczudlik A, Thor PJ.
Klinika Neurologii Instytutu Neurologii Collegium Medicum Uniwersytetu Jagiellonskiego ul. Botaniczna 3, 31-503 Krakow.

Autonomic dysfunction in idiopathic Parkinson's disease (IPD) is common and occurs in 70% of patients. The aim of the study was to evaluate autonomic mechanisms regulating cardiovascular system during tilt up test in IPD patients. The examination was performed in 35 patients with IPD (26 male and 9 female, mean age 60 +/- 9) and matched with gender and age 35 controls subjects (healthy volunteers, mean age 59 +/- 9). Patients were divided into two groups: group I--early stage of disease (n = 20) and group II--advanced stage of the disease (n = 15). The tilt test in IPD patients and in the control group lasted 3 minutes. In both groups tilt test was performed with a head-up tilt position of 60 degrees (tilt table Manumed, Netherlands). In both groups 30:15 ratio were lower than in the control group 1.03 +/- 0.08, 0.97 +/- 0.09 v 1.23 +/- 0.1 respectively (p = 0.001). In the second group the heart-rate variability after the tilt test was lower 6.2 +/- 4/min than in the control group 10.2 +/- +/- 1.9/min and group I 8.8 +/- 4/min (p = 0.01). The decrease of the systolic pressure in response to the tilt test was the highest in group II (16 +/- 14 mmHg), in the control group 4 +/- 7 mmHg, in group I 13 +/- 11 mmHg (p = 0.001). Ortostatic hypotension in IPD occurs in 36% of patients in an early stage and in 47% of patients in an advanced stage of the disease. The use of the tilt test enables the early diagnosis of cardiovascular disturbances in IPD.


Nervenarzt. 2003 Mar;74 Suppl 1:S7-11.
Methods for the early diagnosis of Parkinson's disease
Becker G.
Nervenklinik und Poliklinik,Neurologie, Universitatskliniken des Saarlandes,Homburg/Saar.

Patients with idiopathic Parkinson's disease display a 60% degeneration of the nigrostriatal neurons before motor symptoms have progressed enough to allow clinical diagnosis. It is clear that any neuroprotective therapy starting at such a late stage can have no substantial effect on the disease progression. Therefore, earlier diagnosis must be the goal of future research,when at most mild motor or non-motor symptoms are present or when only risk factors can be identified. Evidence of various gene mutations associated with idiopathic Parkinsonism raise the hope that these or other biological markers will allow earlier identification of patients at risk. A possibly significant vulnerability factor for developing Parkinson's disease can also be demonstrated by means of transcranial sonography. Since the individual tests are not sufficiently specific or sensitive, a gradual, precise, and inexpensive battery of tests needs to be developed for the successful identification of a risk group for this disease. The extent of damage to the dopaminergic system in these patients can be quantified using nuclear techniques.


Arch Intern Med. 2002 Dec 9-23;162(22):2589-93.
Plasma measurement of D-dimer levels for the early diagnosis of ischemic stroke subtypes.
Ageno W, Finazzi S, Steidl L, Biotti MG, Mera V, Melzi D'Eril G, Venco A.
Divisione di Medicina Interna, Ospedale di Circolo, Universita dell'Insubria, Viale Borri 57, 21100 Varese, Italy.

BACKGROUND: Different coagulation abnormalities according to stroke subtypes have been reported. We have assessed the clinical utility of D-dimer, a product of fibrin degradation, in the early diagnosis of stroke subtypes. METHODS: Patients hospitalized after an acute ischemic cerebrovascular event underwent D-dimer assay (STA Liatest D-Dimer) (reference level, <0.50 micro g/mL) on days 1, 6 +/- 1, and 12 +/- 1 and were studied to identify stroke subtypes. RESULTS: We included 126 patients (mean age, 75.5 years) and 63 age-matched control subjects. Stroke subtypes were cardioembolic in 34 patients (27%), atherothrombotic in 34 (27%), lacunar in 31 (25%), and unknown in 27 (21%). At all 3 measurements, D-dimer levels were significantly higher in the cardioembolic group (mean +/- SEM, 2.96 +/- 0.51, 2.58 +/- 0.40, and 3.79 +/- 0.30 micro g/mL, respectively) than in the atherothrombotic (1.34 +/- 0.21, 1.53 +/- 0.26, and 2.91 +/- 0.23 micro g/mL, respectively) (P<.05) and lacunar (0.67 +/- 0.08, 0.72 +/- 0.15, and 0.64 +/- 0.06 micro g/mL, respectively) groups (P<.01). The difference was also significant between the latter 2 groups (P<.01). We found no difference between the lacunar group and controls (0.53 +/- 0.14 micro g/mL). According to day 1 measurements, the optimal cutoff point for predicting cardioembolic stroke was 2.00 micro g/mL, resulting in a specificity of 93.2% and in a sensitivity of 59.3%. For predicting lacunar stroke, the cutoff point was 0.54 micro g/mL, with a specificity of 96.2% and a sensitivity of 61.3%. CONCLUSION: The increasing use of the D-dimer assay in clinical practice could be extended to patients presenting with acute cerebrovascular ischemic events to help predict stroke subtype.


Mov Disord. 2001 Jan;16(1):41-6.
Loss of olfaction in de novo and treated Parkinson's disease: possible implications for early diagnosis.
Tissingh G, Berendse HW, Bergmans P, DeWaard R, Drukarch B, Stoof JC, Wolters EC.
Research Institute Neurosciences Vrije Universiteit, Department of Neurology, Vrije Universiteit Medical Center, Amsterdam, The Netherlands.

Olfactory dysfunction is a common finding in patients with Parkinson's disease (PD). As most studies reported on odor identification in more advanced and treated PD, we administered an odor detection, discrimination, and identification test to a heterogeneous, partly de novo, group of patients. Forty-one non-demented PD patients, 24 of whom had untreated early PD, and 18 healthy controls, were examined. Odor identification and discrimination data were corrected for odor detection scores. PD patients scored significantly lower on all olfactory tests. Interestingly, the subgroup of de novo patients with early PD also showed significant olfactory disturbances compared with healthy subjects. Within the PD group, using multiple regression analysis, we found a significant, negative correlation between odor discrimination measures and disease The present study is the first to describe decreased performance of PD patients on odor discrimination, in addition to the already well-established deficits in odor detection and identification. Furthermore, odor discrimination measures were related to disease severity, possibly indicating that at least some aspects of olfactory dysfunction in PD may be secondary to ongoing degenerative processes in PD. As significant olfactory impairments were found in early, de novo PD, olfactory tests may be useful in the early diagnosis of PD.


J Neurol. 2002 Oct;249 Suppl 3:III/40-8.
Early diagnosis of Parkinson's disease.
Becker G, Muller A, Braune S, Buttner T, Benecke R, Greulich W, Klein W, Mark G, Rieke J, Thumler R.
Department of Neurology, University of Saarland, Gebaude 90, 66421 Homburg/Saar, Germany.

In idiopathic Parkinson's disease (IPD) approximately 60 % of the nigrostriatal neurons of the substantia nigra (SN) are degenerated before neurologists can establish the diagnosis according to the widely accepted clinical diagnostic criteria. It is conceivable that neuroprotective therapy starting at such an 'advanced stage' of the disease will fail to stop the degenerative process. Therefore, the identification of patients at risk and at earlier stages of the disease appears to be essential for any successful neuroprotection. The discovery of several genetic mutations associated with IPD raises the possibility that these, or other biomarkers, of the disease may help to identify persons at risk of IPD. Transcranial ultrasound have shown susceptibility factors for IPD related to an increased iron load of the substantia nigra. In the early clinical phase, a number of motor and particularly non-motor signs emerge, which can be identified by the patients and physicians years before the diagnosis is made, notably olfactory dysfunction, depression, or 'soft' motor signs such as changes in handwriting, speech or reduced ambulatory arm motion. These signs of the early, prediagnostic phase of IPD can be detected by inexpensive and easy-to-administer tests. As one single instrument will not be sensitive enough, a battery of tests has to be composed measuring independent parameters of the incipient disease. Subjects with abnormal findings in this test battery should than be submitted to nuclear medicine examinations to quantify the extent of dopaminergic injury and to reach the goal of a reliable, early diagnosis.


Ann Neurol. 1998 Sep;44(3 Suppl 1):S10-8.
The early diagnosis of Parkinson's disease.
Brooks DJ.
MRC Cyclotron Unit, Hammersmith Hospitals, London, United Kingdom.

Current accepted clinical criteria for the diagnosis of Parkinson's disease (PD) provide high sensitivity for detecting parkinsonism but generally show poor specificity for identifying brainstem Lewy body disease. Biochemical markers that can be used to reliably diagnose clinical and preclinical PD have thus far been sought unsuccessfully. It is now known that some PD kindreds have a mutation of the alpha-synuclein gene, but this cannot be used as a genetic marker for most familial and sporadic cases. Functional imaging provides a means of discriminating typical from atypical PD, revealing characteristic patterns of loss of dopaminergic function. In addition, PET and SPECT show preserved levels of striatal metabolism and dopamine receptor binding in PD, whereas levels are reduced in the atypical variants. [18F]Dopa PET can also detect preclinical PD. In one series there was a reported 40% prevalence of preclinical dopaminergic dysfunction in asymptomatic adult relatives of familial PD patients. Finally, PET and SPECT can both be used to follow PD progression objectively. Such studies suggest an annual 4 to 12% loss of dopamine terminal function in early PD and a preclinical disease window of only a few years. In the future, functional imaging is likely to play an increasingly important role in assessing the efficacy of putative neuroprotective agents.


Neurology. 1995 Nov;45(11):1995-2004.
Early differential diagnosis of Parkinson's disease with 18F-fluorodeoxyglucose and positron emission tomography.
Eidelberg D, Moeller JR, Ishikawa T, Dhawan V, Spetsieris P, Chaly T, Belakhlef A, Mandel F, Przedborski S, Fahn S.
Department of Neurology, North Shore University Hospital/Cornell University Medical College, Manhasset, NY 11030, USA.

Early-stage Parkinson's disease (EPD) is often clinically asymmetric. We used 18F-fluorodeoxyglucose (FDG) and PET to assess whether EPD can be detected by a characteristic pattern of regional metabolic asymmetry. To identify this pattern, we studied 10 EPD (Hoehn and Yahr stage I) patients (mean age 61.1 +/- 11.1 years) using 18F-FDG and PET to calculate regional metabolic rates for glucose. The scaled subprofile model (SSM) was applied to metabolic asymmetry measurements for the combined group of EPD patients and normal subjects to identify a specific covariation pattern that discriminated EPD patients from normal subjects. To determine whether this pattern could be used diagnostically, we studied a subsequent group of five presumptive EPD patients (mean age 50.9 +/- 18.3), five normal subjects (mean age 44.6 +/- 15.3), and nine patients with atypical drug-resistant early-stage parkinsonism (APD) (mean age 44.6 +/- 14.0). In each member of this prospective cohort, we calculated the expression of the EPD-related covariation pattern (subject scores) on a case-by-case basis. We also studied 11 of the EPD patients, five patients with APD, and 10 normal subjects with 18F-fluorodopa (FDOPA) and PET to measure presynaptic nigrostriatal dopaminergic function, and we assessed the accuracy of differential diagnosis with both PET methods using discrimination analysis. SSM analysis disclosed a significant topographic contrast profile characterized by covariate basal ganglia and thalamic asymmetries. Subject scores for this profile accurately discriminated EPD patients from normal subjects and APD patients (p < 0.0001). Group assignments into the normal or parkinsonian categories with FDG/PET were comparable to those achieved with FDOPA/PET, although APD and EPD patients were not differentiable by the latter method. Metabolic brain imaging with FDG/PET may be useful in the differential diagnosis of EPD.


Neurology. 1993 Dec;43(12 Suppl 6):S6-16.
PET studies on the early and differential diagnosis of Parkinson's disease.
Brooks DJ.
MRC Cyclotron Unit, Hammersmith Hospital, London, U.K.

A number of neurodegenerative diseases can manifest as parkinsonian disorders. Structural imaging, such as CT and MRI, is of limited value for differentiating these diseases. PET can demonstrate the selective patterns of disruption of regional cerebral metabolism and neurotransmitter systems associated with subcortical degenerations, such as Parkinson's disease, striatonigral degeneration, progressive supranuclear palsy, and corticobasal degeneration. It can also determine, where underlying Parkinson's disease may be suspected, whether nigral dysfunction is present in patients with isolated tremor or drug-associated rigidity. Finally, PET can detect the presence of subclinical disruption of the dopaminergic system in at-risk subjects, such as relatives of patients with Parkinson's disease, or subjects exposed to nigral toxins, such as MPTP. With the advent of putative neuroprotective agents for Parkinson's disease, PET can help identify patients with early disease who might benefit from therapy with these agents and monitor their disease progression.


Neurology. 1991 May;41(5 Suppl 2):50-1; discussion 52.
Catechol metabolites in the cerebrospinal fluid as possible markers in the early diagnosis of Parkinson's disease.
Carlsson A, Fornstedt B.
Department of Pharmacology, University of Gothenburg, Sweden.

This paper is a preliminary report of work aiming to elucidate the possible use of 5-S-cysteinyl metabolites of catechols in the cerebrospinal fluid as markers in the early diagnosis of Parkinson's disease (PD). The rationale for this approach is the hypothesis that this disorder is caused by a failure of antioxidative mechanisms to prevent the excessive autoxidation of dopamine and other catechols that yields highly reactive and cytotoxic semiquinones and quinones. 5-S-cysteinyl adducts of these quinones have been detected in human brains, analyzed postmortem, and appear to be formed at an increased rate in elderly individuals, who show an increased loss of dopaminergic neurons.


Versicherungsmedizin. 1997 Aug 1;49(4):126-31.
Effect of early diagnosis and therapy on prognosis of Parkinson syndrome
Werner M, Fornadi F.
Gertrudis-Klinik Biskirchen, Parkinson-Zentrum.

Parkinson's disease is a chronic-progressive neuro-degenerative syndrome, which should be diagnosed as early as possible because of the therapeutic success in the beginning. Knowing the initial symptoms and using modern technical devices like SPECT and PET we shall be able to influence the course and the prognosis of the disease positively. The application of a current combined drug-therapy and in addition physiotherapy, speech-therapy and psychotherapy enable us to provide quality of life or to restore it. Repeated treatments in Parkinson medical centers intensify the efficacy of therapeutic efforts. Nevertheless even in early stages patients and physicians can be confronted with social medical problems like defining the degree of disability or the time for receiving a pension. The knowledge of specific disease-related findings will help to judge all these problems in accordance with the needs of the patients.

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

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

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