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ANTI-AGING BIOMEDICINE.
HIGH TECH BIO-MEDICAL TECHNOLOGIES FOR DISEASE TREATMENT AND LIFE EXTENSION.
EXPERIMENTAL AND CLINICAL DATA.

 
 6.1 Alzheimer's disease and Dementia 
   
 
Cerebrospinal fluid biochemical markers in early detection and in differential diagnosis of dementia disorders in routine clinical practice.
Clinical Value of Neuroimaging in the Diagnosis of Dementia. Sensitivity and Specificity of Regional Cerebral Metabolic and Other Parameters for Early Identification of Alzheimer's Disease.
Biomarkers, mild cognitive impairment and early diagnosis of Alzheimer's disease.
Amnestic behavior in dementia: symptoms to assist in early detection and diagnosis.
The role of biological markers in the early and differential diagnosis of Alzheimer's disease.
Early diagnosis, therapy, and long-term follow up of dementia.
Preimplantation diagnosis for early-onset Alzheimer disease caused by V717L mutation.
Magnetization transfer measurements of the hippocampus in the early diagnosis of Alzheimer's disease.
Early diagnosis of dementia.
 
   
   
Neurol Sci. 2003 Oct;24(3):199-200.
Cerebrospinal fluid biochemical markers in early detection and in differential diagnosis of dementia disorders in routine clinical practice.
Parnetti L, Lanari A, Saggese E, Spaccatini C, Gallai V.
Memory Clinic, Alzheimer Center, Department of Neuroscience, University of Perugia, Perugia, Italy.

Measurement of total tau and amyloid beta1-42 (Ab42) in cerebrospinal fluid (CSF) improves diagnostic accuracy of Alzheimer's disease (AD). We examined a consecutive patient sample referred to our center for diagnostic assessment of cognitive decline. CSF tau and Abeta42 were assayed each week as routine neurochemical analyses. There were 119 patients investigated. These included 61 with probable AD (35 mild AD, 26 severe AD), 24 with mild cognitive impairment (MCI), 14 with vascular dementia, 11 with Lewy body dementia, and 9 with fronto-temporal dementia. Mild AD showed significantly lower CSF Abeta42 levels and significantly higher CSF tau levels than the other diagnostic groups; 79% of MCI patients had pathological values for both biomarkers. We confirm that these biomarkers have a role in the clinical work-up of patients with cognitive deficits.

   
   

Clin Positron Imaging. 1999 May;2(3):119-130.
Clinical Value of Neuroimaging in the Diagnosis of Dementia. Sensitivity and Specificity of Regional Cerebral Metabolic and Other Parameters for Early Identification of Alzheimer's Disease.
Silverman DH, Small GW, Phelps ME.
Department of Molecular and Medical Pharmacology, University of California, Los Angeles, School of Medicine, Los Angeles, CA, USA

Dementing illnesses such as Alzheimer's disease (AD) progressively devastate human brain tissue and consequently the health and lives of people afflicted by these disorders. One of the greatest clinical challenges posed by dementia is establishing an approach to ensure its early identification and accurate diagnosis-thus making it possible to treat and, potentially, arrest the development of disease before a substantial amount of brain tissue has been permanently destroyed. The data generated by neuroimaging studies conducted over the past two decades show PET with [(18)F]fluorodeoxyglucose (FDG) to be exceptionally well-suited to meeting this challenge. The regional metabolic patterns imaged with FDG-PET enable sensitive diagnosis of AD, and reveal pathophysiologic alterations even before they lead to symptomatic expression. The accuracy of PET in identifying early AD, and distinguishing it from other etiologies of cognitive impairment, exceeds that of CT, MRI (qualitative or quantitative), and SPECT, as well as that of expert clinical evaluation based on history, physical examination, cognitive testing, and blood laboratory values. Recent developments in instrumentation and radiopharmaceutical distribution have made obtaining scans of cerebral metabolism achievable in routine clinical settings, including most hospitals in which Nuclear Medicine services are provided, for less than the cost of a single year of anticholinesterase therapy or a single month of lost productivity. The need and opportunity are thus present for making a fundamental change in the current approach to evaluating patients for dementia.

   
   

Nippon Ronen Igakkai Zasshi. 2003 Jan;40(1):22-6.
Biomarkers, mild cognitive impairment and early diagnosis of Alzheimer's disease
Arai H.
Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine.

Elderly people are concerned about changes in their cognitive functioning. Since cholinergic therapies for Alzheimer's disease have been developed and become widely accepted, elderly people have come to visit clinics to seek medical advice about whether such a subtle change in cognitive ability may represent an early manifestation of Alzheimer's disease (AD). If they are likely to develop dementia or AD, they want to receive immediate medical treatment as soon as possible to prevent further loss of cognitive functioning so that they can live independently as long as possible. The first priority in the clinical application of a biomarker is that biomarker should contribute to early diagnosis of dementia. Among such biomarkers, we believe that cerebrospinal fluid markers and functional brain imaging are clinically the most applicable procedures. Since 1993, we have collected 623 cerebrospinal fluid (CSF) samples at The Tohoku University Hospital for evaluation of dementia (age: 42-93). We found that CSF/phospho-tau measures produced the most adequate sensitivity (85.2%) and specificity (85.0%) in the diagnosis of AD as a sole bio-marker. The CSF levels of A beta 1-42 showed a strong positive correlation with the Mini-mental state examination score and brain glucose metabolism by positron emission tomography. The baseline levels of both total-tau and phospho-tau in CSF increased in approximately 70% of patients with mild cognitive impairment who later developed AD, suggesting that pathological change in the brain might start years before dementia becomes clinically manifested. A combined use of CSF-tau and IMP-SPECT improved the predictability of the transition from mild cognitive impairment into AD.

   
   

J Am Geriatr Soc. 2003 Jan;51(1):32-7.
Amnestic behavior in dementia: symptoms to assist in early detection and diagnosis.
Ready RE, Ott BR, Grace J.
Department of Psychiatry and Human Behavior, Brown University School of Medicine, Pawtucket, Rhode Island, USA.

OBJECTIVES: This study evaluated two amnestic behavior changes (repetitive questioning and repetitive actions) to determine their utility in screening for early dementia. DESIGN: Patient data were collected through a retrospective chart review. Comparison data from nondemented older people were collected prospectively from acquaintances of clinic patients. SETTING: The setting was a hospital-based outpatient memory disorder clinic. PARTICIPANTS: Participants were older individuals with no cognitive impairment (n = 25), undetermined dementia (n = 50), and definite dementia (n = 25). The undetermined cases were followed for at least 1 year to assess for conversion to dementia. MEASUREMENTS: Amnestic behaviors were assessed using informant-report for all participants. The behaviors were examined for their ability to distinguish between definite dementia cases and noncases. They were further evaluated for the ability to differentiate undetermined cases that eventually converted to definite dementia from cases that did not convert. RESULTS: Results indicated that repetitive behaviors were common in early and more-severe dementia cases. Repetitive behaviors were relatively uncommon in cognitively intact older participants. In analyses of the full study sample, engagement in repetitive behaviors had high sensitivity (0.97) in identifying dementia cases. CONCLUSIONS: Assessing repetitive behaviors in patients may be a useful means for family members and primary care physicians to screen for early cognitive impairment. The assessment can help to identify individuals that should be evaluated further for dementia.

   
   

J Neural Transm Suppl. 2002;(62):127-33.
The role of biological markers in the early and differential diagnosis of Alzheimer's disease.
Kurz A, Riemenschneider M, Drzezga A, Lautenschlager N.
Department of Psychiatry, Technische Universitat Munchen, Federal Republic of Germany.

Biological markers can be used to identify the neurodegenerative process of Alzheimer's disease (AD) and to differentiate it from other brain diseases which may cause similar symptoms. Structural imaging can detect atrophic changes which are largely non-specific and provide little diagnostic information in single patients. Increasing atrophy upon repeated measurement is much more specific to AD. Functional imaging can demonstrate regional alterations of cerebral blood flow and metabolism but is not sufficiently sensitive at the stage of mild dementia. The measurement of neuronal proteins in the cerebrospinal fluid including tau, phospho-tau, and beta amyloid, achieve high diagnostic sensitivity and specificity even at the stage of pre-dementia. Genetic tests for mutations in the amyloid precursor and presenilin genes are applicable in very few cases. Apolipoprotein E genotyping is not useful as a diagnostic test. With respect to the limitations of biological markers clinical expertise will continue to be an essential element of the early and differential diagnosis of AD.

   
   

Nippon Ronen Igakkai Zasshi. 2002 May;39(3):282-5.
Early diagnosis, therapy, and long-term follow up of dementia
Takechi H.
Department of Geriatric Medicine, Graduate School of Medicine, Kyoto University.

Since the start of long term care insurance and the availability of cholinesterase inhibitor as a prescription drug in Japan, detection and diagnosis of dementia in the early stage of the disease has become an important issue. Neuropsychological screening and imaging tools usually employed for diagnosis are insufficient. The use of diagnostic criteria to designate early stage patients is still controversial. Several disease entities, including mild cognitive impairment (MCI) and age-associated memory impairment (AAMI), are not clearly defined in Japan. To study the prognosis of early stage dementia, it is important to define the diagnostic criteria. Clear identification and diagnosis of early stage dementia is important to support patients and their family members. The early detection of dementia and cognitive decline has other important aspects. One is the implication of disease diagnosis in the community; people often hesitate to use the name dementia in the early stage, even when the patients fulfill the criteria for dementia. Another aspect is the longer term follow up of the patients after early detection. For these purposes, it will become more important to emphasize a team approach consisting of medical doctors, nurses, neuropsychologists, clinical psychologists, occupational therapists and socialteam workers.

   
   

JAMA. 2002 Feb 27;287(8):1018-21.
Preimplantation diagnosis for early-onset Alzheimer disease caused by V717L mutation.
Verlinsky Y, Rechitsky S, Verlinsky O, Masciangelo C, Lederer K, Kuliev A.
Reproductive Genetics Institute, Chicago, IL, USA.

CONTEXT: Indications for preimplantation genetic diagnosis (PGD) have recently been expanded to include disorders with genetic predisposition to allow only embryos free of predisposing genes to be preselected for transfer back to patients, with no potential for pregnancy termination. OBJECTIVE: To perform PGD for early-onset Alzheimer disease (AD), determined by nearly completely penetrant autosomal dominant mutation in the amyloid precursor protein (APP) gene. DESIGN: Analysis undertaken in 1999-2000 of DNA for the V717L mutation (valine to leucine substitution at codon 717) in the APP gene in the first and second polar bodies, obtained by sequential sampling of oocytes following in vitro fertilization, to preselect and transfer back to the patient only the embryos that resulted from mutation-free oocytes. SETTING: An in vitro fertilization center in Chicago, Ill. PATIENTS: A 30-year-old AD-asymptomatic woman with a V717L mutation that was identified by predictive testing of a family with a history of early-onset AD. MAIN OUTCOME MEASURES: Results of mutation analysis; pregnancy outcome. RESULTS: Four of 15 embryos tested for maternal mutation in 2 PGD cycles, originating from V717L mutation--free oocytes, were preselected for embryo transfer, yielding a clinical pregnancy and birth of a healthy child free of predisposing gene mutation according to chorionic villus sampling and testing of the neonate's blood. CONCLUSION: This is the first known PGD procedure for inherited early-onset AD resulting in a clinical pregnancy and birth of a child free of inherited predisposition to early-onset AD.

   
   

J Neurol Sci. 2001 Jul 15;188(1-2):79-84.
Magnetization transfer measurements of the hippocampus in the early diagnosis of Alzheimer's disease.
Hanyu H, Asano T, Sakurai H, Takasaki M, Shindo H, Abe K.
Department of Geriatric Medicine, Tokyo Medical University, 6-7-1 Nishishinjuku, Shinjuku-ku, 160-0023, Tokyo, Japan.

We measured magnetization transfer ratios (MTRs) of the hippocampus in 38 patients with Alzheimer's disease (AD), including very mild (Clinical Dementia Rating [CDR] 0.5, n=12), mild (CDR 1, n=14), and moderate stages (CDR 2, n=12), and in 21 healthy elderly control subjects. Medial temporal lobe atrophy was graded subjectively on a five-point scale by two observers blinded to clinical data. Compared with the controls, each of the AD groups, including the very mild group, had significant atrophy of the medial temporal lobe and a decrease in MTRs of the hippocampus. Logistic regression analysis revealed that the overall discrimination rate with MTR measurement and visual analysis of the atrophy was 85% and 73% between the control group and the CDR 0.5 group, 89% and 80% between the control group and the CDR 1 group, and 100% and 91% between the control group and the CDR 2 group, respectively. MTR measurements may provide additional information in detecting structural damage of the hippocampus of AD and be helpful in providing improved diagnosis and early detection of AD.

   
   

Am Fam Physician. 2001 Feb 15;63(4):703-13, 717-8.
Early diagnosis of dementia.
Santacruz KS, Swagerty D.
University of Kansas Medical Center, Kansas City, USA.

Until recently, the most significant issue facing a family physician regarding the diagnosis and treatment of dementia was ruling out delirium and potentially treatable etiologies. However, as more treatment options become available, it will become increasingly important to diagnose dementia early. Dementia may be suspected if memory deficits are exhibited during the medical history and physical examination. Information from the patient's family members, friends and caregivers may also point to signs of dementia. Distinguishing among age-related cognitive decline, mild cognitive impairment and Alzheimer's disease may be difficult and requires evaluation of cognitive and functional status. Careful medical evaluation to exclude treatable causes of cognitive impairment is important. Patients with early dementia may benefit from formal neuropsychologic testing to aid in medical and social decision-making. Follow-up by the patient's family physician is appropriate in most patients. However, a subspecialist may be helpful in the diagnosis and management of patients with dementia with an unusual presentation or following an atypical course.

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FASTING / LOW CALORIE PROGRAMS
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)
        Obesity
Diabetes
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
Allergies
Rheumatoid arthritis
Gastrointestinal diseases
Infertility
Presbyacusis
    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
Radio-sensitivity
Apoptosis
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
     

Vegetables
Fruits
Bread, cereals, pasta, fiber
Glycemic index
Fish
Meat and poultry
Sugar and sweet
Legumes
Fats and oils
Dairy and eggs
Mushrooms
Nuts and seeds
Alcohol
Coffee
Water
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
Selenium
Flavonoids, carotenes
DHEA
Vitamin B
Carnitin
SAM
Vinpocetine (Cavinton)
Deprenyl (Eldepryl)
    5.2 Drugs with controversial or unproven anti-aging effect, or awaiting other evaluation (side-effects)
        Phyto-medicines, Herbs
HGH
Gerovital
Melatonin
      5.3 Drugs for treatment and prevention of specific diseases of aging. High-tech modern pharmacology.
        Alzheimer's disease and Dementia
Arthritis
Cancer
Depression
Diabetes
Hyperlipidemia
Hypertension
Immune decline
Infections, bacterial
Infections, fungal
Memory loss
Menopause
Muscle weakness
Osteoporosis
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
Arthritis
Cancer
Depression
Diabetes
Cataracts and Glaucoma
Genetic disorders
Heart attacks
Hyperlipidemia
Hypertension
Immune decline
Infectious diseases
Memory loss
Muscle weakness
Osteoporosis
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
        Blood
Bones, limbs, joints etc.
Brain
Heart & heart devices
Kidney
Liver
Lung
Pancreas
Spleen
    6.6 Obesity reduction by ultrasonic treatment
  Physical activity and aging. Experimental and clinical data.
        Aerobic exercises
Stretching
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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