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100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
100 Years of Alzheimer's Disease: Prevention, Cure, Care
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100 Years of Alzheimer's Disease: Prevention, Cure, Care

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    1. 100 Years of Alzheimer’s Disease: Prevention, Cure, Care <ul><li>Marilyn S. Albert, PhD </li></ul><ul><li>Department of Neurology </li></ul><ul><li>Johns Hopkins University </li></ul>
    2. Summary - Epochs of Progress <ul><li>100 years ago – unknown as a disease </li></ul><ul><li>30 years ago – no research effort </li></ul><ul><li>15 years ago – no known genes associated with AD, limited understanding of biological pathways </li></ul><ul><li>10 years ago – no animal models of disease </li></ul><ul><li>5 years ago – no prevention trials funded, limited ability to identify persons at high risk, limited knowledge about factors that promote brain health </li></ul>
    3. Overview of Recent Progress Hope for Tomorrow <ul><li>Genetics Provides Clues for Drug Development </li></ul><ul><li>Clinical Research Emphasizes Importance of Early Diagnosis </li></ul><ul><li>Technology Provides Methods for Tracking Evolution of Disease </li></ul><ul><li>Population Studies Provide Clues to Factors that Promote Brain Health </li></ul>
    4. Status of Alzheimer’s Disease 30 Years Ago <ul><li>AD considered a rare disease (early onset) </li></ul><ul><li>Handful of investigators interested in the area (research budget virtually zero) </li></ul><ul><li>AD considered untreatable and hopeless </li></ul><ul><li>No specialized clinical professionals or clinical facilities </li></ul><ul><li>No broadly accepted criteria for diagnosis or methods of assessment </li></ul><ul><li>No sources of information and support for patients and families </li></ul>
    5. Major Accomplishments 1970s-1980s <ul><li>AD associated with specific pathological changes in the brain (clinical pathological correlations) </li></ul><ul><li>AD associated with specific biochemical changes in the brain (acetylcholine deficiency) </li></ul><ul><li>Consensus on clinical and pathological criteria for diagnosis </li></ul>
    6. Pathophysiology of AD ~ 1975-1990s <ul><li>Neuritic plaques </li></ul><ul><li>Neurofibrillary tangles </li></ul><ul><li>Synaptic & neuronal loss </li></ul><ul><li>Neurotransmitters ( acetylcholine ) </li></ul><ul><li>temporal parietal frontal </li></ul>
    7.  
    8.  
    9. ‘ Definite’ Diagnosis of AD ‘gold standard’ <ul><li>Presence of dementia during life </li></ul><ul><li>Examination of brain tissue to determine prevalence of neuritic plaques and neurofibrillary tangles </li></ul>
    10.  
    11. Clinical Diagnosis of AD ‘ Probable or Possible AD’ <ul><li>History of progressive decline in two or more areas of cognition (e.g., memory, language, spatial ability, executive function) </li></ul><ul><li>Laboratory tests to identify treatable or structural causes of dementia (e.g., CBC, TFTs, LFTs, RPR, CT or MRI) </li></ul><ul><li>Consciousness not clouded (i.e., absence of acute confusion) </li></ul><ul><li> ~ 90 % accurate </li></ul><ul><li> McKhann et al., 1984 </li></ul><ul><li> </li></ul>
    12. Pathophysiology of AD ~ 1975-1990s <ul><li>Neuritic plaques </li></ul><ul><li>Neurofibrillary tangles </li></ul><ul><li>Synaptic & neuronal loss </li></ul><ul><li>Neurotransmitters ( acetylcholine ) </li></ul><ul><li>temporal parietal frontal </li></ul>
    13. Current Treatments for AD <ul><li>Aricept (donepezil): 5-10mg qd * </li></ul><ul><li>Exelon (rivastigmine): 3-6mg bid * </li></ul><ul><li>Reminyl (galantamine): 4-12mg bid * </li></ul><ul><li>Ebixa (memantine): 5-20mg qd </li></ul><ul><li>~ 6 month improvement in function </li></ul><ul><li>* - cholinesterase inhibitors </li></ul>
    14.  
    15.  
    16. A Disease Modifying Agent Would Alter Rate of Progression <ul><li>No Treatment </li></ul>Time Cognitive Function Early Treatment
    17. Major Accomplishments 1990s <ul><li>Molecular structure of the hallmark brain abnormalities (plaques and tangles) identified </li></ul><ul><li>Genetic mutations identified that cause early onset form of disease (Ch. 21, 14, 1 – APP, PS1, PS2) </li></ul><ul><li>Genetic variant identified that increases susceptibility to disease (APOE) </li></ul>
    18. Molecular pathology of AD: plaques <ul><li>Primary component is Aß, a 40 or 42 amino acid peptide derived from APP </li></ul><ul><li>Numerous other components including apoE and a2M </li></ul><ul><li>Sponge-like aggregate in the neuropil includes cellular elements </li></ul><ul><li>Glial response near many plaques </li></ul>
    19. Molecular pathology of AD: tangles <ul><li>Paired helical filaments by EM </li></ul><ul><li>Microtubule associated protein tau is major component </li></ul><ul><li>20-25 phosphorylation sites identified </li></ul><ul><li>Kinases are a therapeutic target </li></ul>
    20. Search for Genetic Factors that Cause Alzheimer’s Disease <ul><li>Identify families in which AD occurs in large numbers across multiple generations </li></ul><ul><li>Obtain clinical information and blood for genetic analysis from families </li></ul><ul><li>Identify location of gene shared by individuals with disease vs those without </li></ul><ul><li>Determine specific genetic mutation that causes disease </li></ul>
    21.  
    22. Role of Genetics in AD <ul><li>Early Onset AD </li></ul><ul><ul><li>(Onset < 60 - 65 yrs) </li></ul></ul><ul><ul><ul><li>Chromosome 21 - APP Gene </li></ul></ul></ul><ul><ul><ul><li>Chromosome 14 - PS1 Gene </li></ul></ul></ul><ul><ul><ul><li>Chromosome 1 - PS2 Gene </li></ul></ul></ul><ul><li>Late Onset AD </li></ul><ul><ul><li>(Onset > 60 - 65 yrs) </li></ul></ul><ul><ul><ul><li>Chromosome 19 - APOE Gene </li></ul></ul></ul><ul><ul><ul><ul><li>3 alleles - APOE 2, 3, 4 </li></ul></ul></ul></ul><ul><ul><ul><ul><li>APOE-4 increases susceptibility </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>to AD </li></ul></ul></ul></ul></ul>
    23. Development of Mice Carrying Major Genes for AD sac Y Y Y Y Y Mice Appear Normal Plaques Develop Memory Deficit Emerges
    24. Spatial Memory Task
    25. Alzheimer’s Disease Genes Early Onset AD (Onset <60 years)
    26. A β misfolding into “amyloid”
    27. Dominant Genes Suggest Mechanism - based on ‘Amyloid Hypothesis’ - <ul><li>Dominant AD genes increase production of beta-amyloid protein (A ß 1-42) - beta secretase and gamma secretase </li></ul><ul><li>Beta amyloid protein accumulates, generating neuritic plaques </li></ul><ul><li>Neurofibrillary tangle formation accelerates </li></ul><ul><li>Synaptic and neuronal loss progresses </li></ul>
    28. Role of Genetics in AD <ul><li>Early Onset AD </li></ul><ul><ul><li>(Onset < 60 - 65 yrs) </li></ul></ul><ul><ul><ul><li>Chromosome 21 - APP Gene </li></ul></ul></ul><ul><ul><ul><li>Chromosome 14 - PS1 Gene </li></ul></ul></ul><ul><ul><ul><li>Chromosome 1 - PS2 Gene </li></ul></ul></ul><ul><li>Late Onset AD </li></ul><ul><ul><li>(Onset > 60 - 65 yrs) </li></ul></ul><ul><ul><ul><li>Chromosome 19 - APOE Gene </li></ul></ul></ul><ul><ul><ul><ul><li>3 alleles - APOE 2, 3, 4 </li></ul></ul></ul></ul><ul><ul><ul><ul><li>APOE-4 increases susceptibility </li></ul></ul></ul></ul><ul><ul><ul><ul><ul><li>to AD </li></ul></ul></ul></ul></ul>
    29. Search for Improved Treatments - based on ‘Amyloid Hypothesis’ – APOE Gene Findings <ul><li>APOE-4 allele appears to decrease clearance of A ß 1-42 </li></ul><ul><li>Interaction between vascular risk and risk for AD: increase in cholesterol increases accumulation of A ß 1-42 </li></ul>
    30. Impact of Other Factors in Cell Death <ul><li>Inflammation in response to accumulation of amyloid and tau </li></ul><ul><li>Oxidation facilitating further injury </li></ul><ul><li>Cell viability – protective agents that promote response to injury, cell connectivity, blood flow </li></ul>
    31. Medication Types Under Study by Pharmaceutical Companies <ul><li>Anti-amyloid aggregation </li></ul><ul><li>Anti-tau aggregation </li></ul><ul><li>Improve cellular response to injury (oxidation, inflammation) </li></ul><ul><li>Novel treatments – need information on safety and indication of effectiveness </li></ul>
    32. Clinical Trials of Medications Potential for Disease Modification <ul><li>Alzemed </li></ul><ul><li>Flurizan </li></ul><ul><li>Rosiglitazone </li></ul><ul><li>Vaccine – Monoclonal antibody (AAB-001) </li></ul>
    33. A Disease Modifying Agent Would Alter Rate of Progression <ul><li>No Treatment </li></ul>Time Cognitive Function Early Treatment
    34. Major Accomplishments <ul><li>Understanding that disease takes a long time to evolve over time </li></ul><ul><li>Development of methods for studying disease before symptoms are severe enough to warrant diagnosis of AD </li></ul><ul><li>Applications of technology to study of very early disease </li></ul>
    35. Disease Progression Patho- physiology Progression of Neurodegenerative Diseases Normal Prodromal Clinical Dx
    36.  
    37.  
    38. Changes in Brain in Very Mild AD Neuropathologic Data <ul><li>Formation of neuritic plaques and neurofibrillary tangles neuronal loss </li></ul><ul><li>>30% neuronal loss in entorhinal cortex (major input to hippocampus) </li></ul><ul><li>Gradual spread of plaques and tangles and neuronal loss throughout brain (e.g. superior temproral cortex, anterior cingulate, inferior parietal cortex </li></ul>
    39. Evolution of Pathology in Alzheimer’s Disease CONTROL PRODROMAL AD CLINICAL AD Cognitive Performance 100% Disease Progression years A β NFT/TAU Inflammation
    40. Mild Cognitive Impairment MCI <ul><li>memory complaint / corroborated by informant </li></ul><ul><li>not demented </li></ul><ul><ul><li>preserved general cognitive function </li></ul></ul><ul><ul><li>normal activities of daily living </li></ul></ul><ul><li>memory impaired for age and education (tends to be   1.5 SD) </li></ul><ul><li> Petersen et al., 1999 </li></ul>
    41. Individuals With MCI Develop Clinical AD At A Much Higher Rate Than Normal Elderly
    42. Disease Progression Cognitive Function Therapeutic Implications of Disease Course Normal Prodromal Clinical Dementia Prevent Onset Slow Progression Treat Symptoms & Slow Decline
    43. Disease Progression Cognitive Function Progression of Alzheimer’s Disease Normal Prodromal Clinical Dementia Min V Mild MCI Rx
    44. Disease Progression Cognitive Function Progression of Alzheimer’s Disease Normal Prodromal Clinical Dementia Min V Mild MCI Rx
    45. Disease Progression Cognitive Function Progression of Alzheimer’s Disease Normal Prodromal Clinical Dementia Min V Mild MCI Rx
    46. Major Accomplishments <ul><li>Technological advances make imaging feasible for tracking evolution of disease </li></ul><ul><li>Technological advances make measurement of proteins in brain feasible for tracking evolution of disease </li></ul><ul><li>Recognition that careful tracking of disease may be essential for finding better treatments </li></ul>
    47.  
    48. Entorhinal/Hippocampal ROI’s Entorhinal Cortex Hippocampus
    49. Need Better Biomarkers for Clinical Trials <ul><li>Need measurement of outcome within a reasonable period of time </li></ul><ul><li>Biomarkers under consideration – imaging measures and /or measures from blood and urine </li></ul><ul><ul><li>MRI </li></ul></ul><ul><ul><li>PET </li></ul></ul><ul><ul><li>Plasma A ß </li></ul></ul>
    50. Need Better Biomarkers for Clinical Trials <ul><li>Measures need to be standardized across sites </li></ul><ul><ul><li>Reliable (measured in the same way across sites) </li></ul></ul><ul><ul><li>Feasible (can be measured in large numbers of subjects) </li></ul></ul><ul><li>Optimal measures may vary with stage of disease and modality (e.g., MRI, PET, etc) </li></ul>
    51. Alzheimer’s Disease Neuroimaging Initiative <ul><li>Funded jointly by government, industry, foundations </li></ul><ul><li>Planned jointly by academic centers and industry </li></ul><ul><li>N ovel methods of assessment – imaging (MRI and PET), blood, CSF </li></ul><ul><li>International effort – ADNI sites in US and Canada, Collaborating consortia in Europe and Australia </li></ul><ul><li>Goal to help industry find better drugs faster </li></ul>
    52.  
    53. European ADNI Consortium Stockholm – Wahlund/Winblad Munich – Hampel Bio co-PI Brescia – Frisoni Project PI Toulouse – Vellas Clinical PI Amsterdam – Barkhof/Scheltens MR imag PI Copenhagen - Waldemar Gotheborg – Blennow Bio co-PI Participating Sites
    54. Australia ADNI Consortium Perth Melbourne PARTICIPATING SITES
    55. Major Accomplishments <ul><li>Completion of population studies that identify risk factors for AD </li></ul><ul><li>Understanding that life style factors that are modifiable may alter risk for AD </li></ul><ul><li>Start of national campaigns to alter risk factors for AD (Alzheimer’s Australia, UK, US) </li></ul>
    56. Predictors of Maintenance of Cognition <ul><li>Many large community-based observational studies conducted since early 1990s </li></ul><ul><li>Primary study design </li></ul><ul><ul><li>Examine wide range of factors among individuals with good function </li></ul></ul><ul><ul><li>Follow participants over time </li></ul></ul><ul><ul><li>Identify factors that predict maintenance of cognitive function </li></ul></ul>
    57. Predictors of Maintenance of Cognition <ul><li>Community-based Observational Studies </li></ul><ul><li>Nature of Populations Studied </li></ul><ul><ul><li>Emphasize participants unimpaired when first studied </li></ul></ul><ul><ul><li>Examine elderly only (e.g., 70-80 at baseline) as well as middle aged individuals followed into elderly age range </li></ul></ul><ul><ul><li>Geographically diverse (U.S., Canada, Europe; Urban, Rural) </li></ul></ul>
    58. Examples: Longitudinal Studies n=15,000 <ul><li>MacArthur Study of Successful Aging </li></ul><ul><li>Chicago Health & Aging Project </li></ul><ul><li>North Manhattan Aging Study </li></ul><ul><li>Canadian Study of Health & Aging (Canada) </li></ul><ul><li>Kungsholmen Project (Sweden) </li></ul><ul><li>Berlin Aging Study (Germany) </li></ul><ul><li>Rotterdam Study (Netherlands) </li></ul>Albert et al., 1995 Schmand et al., 1997 Laurin e al., 2001 Scarmeas et al., 2001 Verghese et al., 2003 Wilson et al., 2003, 2005 Weuve et al., 2004 Rovio et al., 2005
    59. Predictors of Maintenance of Cognition <ul><li>Physical activity </li></ul><ul><li>Mental activity </li></ul><ul><li>Social engagement </li></ul><ul><li>Vascular risk factors </li></ul><ul><li>Statistical analysis suggests that these factors may be additive </li></ul><ul><li>Genetics </li></ul>
    60. Physical Activity and Maintenance of Cognition <ul><li>Physical activity – activities involved in daily living </li></ul><ul><ul><li>Blocks walked </li></ul></ul><ul><ul><li>Stairs climbed </li></ul></ul><ul><ul><li>Objects lifted </li></ul></ul><ul><ul><li>Total kilocalories expended </li></ul></ul><ul><li>Relationship after adjusting for potential confounders (co-morbid conditions, functional limitations, smoking, etc) </li></ul>
    61. Physical Activity Potential Mechanisms <ul><li>Stimulation of chemicals that protect and repair the brain (e.g., Brain Derived Neurotrophic Factor - BDNF) </li></ul><ul><li>Stimulation of new nerve cells (i.e. neurogenesis) </li></ul><ul><li>Reduced accumulation of amyloid (increased neprilysin, increased expression of genes for learning and memory, cell survival) </li></ul>
    62. Mental Activity and Maintenance of Cognition <ul><li>Educational Experience - relationship after adjusting for socioeconomic status </li></ul><ul><li>Daily activities that are mentally stimulating– crossword puzzles, books, lectures </li></ul>
    63. Mental Activity Potential Mechanisms <ul><li>Development of increased connections among nerve cells </li></ul><ul><li>Compensation - Alternate brain pathways for performing tasks and solving problems </li></ul>
    64. Psychosocial Factors and Maintenance of Cognition <ul><li>Social engagement </li></ul><ul><li>Feelings of self-worth </li></ul><ul><li>Feelings of self-efficacy </li></ul><ul><li>Mood and anxiety </li></ul>
    65. Psychosocial Factors Potential Mechanisms <ul><li>Modulation of stress hormones </li></ul><ul><li>Increased likelihood of compliance with healthy life-style </li></ul>
    66. Vascular Risk Factors and Maintenance of Cognition <ul><li>Blood Pressure </li></ul><ul><li>Diabetes </li></ul><ul><li>Cholesterol </li></ul><ul><li>Weight </li></ul><ul><li>Smoking </li></ul>
    67. Vascular Risk Factors Potential Mechanisms <ul><li>Small and large artery disease </li></ul><ul><li>Disruption of blood brain barrier </li></ul><ul><li>Inflammation and oxidative stress </li></ul>
    68. Vascular Risk Factors <ul><li>Effects may be additive or multiplicative </li></ul><ul><li>Intervention strategies provide multiple potential benefits (heart and brain) </li></ul><ul><li>Minority populations may demonstrate the greatest benefit as risk factors are more prevalent </li></ul>
    69. Combination of Factors Appears Most Effective <ul><li>Ex. Mental and physical activity in combination </li></ul><ul><ul><li>Statistical demonstration of combined effect </li></ul></ul><ul><ul><li>Animal model - physical activity in enriched environment (rodents) </li></ul></ul><ul><ul><li>Human model – tai chi, exercise bicycle while reading </li></ul></ul>
    70. Increasing Interest <ul><li>Alzheimer’s Australia – ‘Mind Your Mind’ campaign </li></ul><ul><li>Alzheimer’s Society UK – ‘Mind Your Head’ campaign </li></ul><ul><li>Alzheimer’s Association, US – ‘Maintain Your Brain’ campaign </li></ul><ul><li>U.S. National Institutes of Health – Cognitive and Emotional Health Project </li></ul>
    71. General Conclusions: Predictors of Maintenance of Cognition <ul><li>A complex interaction of factors predicts maintenance of cognitive function in older persons </li></ul><ul><li>Evidence suggests combination of factors is more effective than any one factor alone </li></ul><ul><li>Results have implications for intervention efforts aimed at minimizing or preventing cognitive decline in older age </li></ul><ul><li>The most effective interventions will likely combine educational activities, physical training, and psychosocial approaches </li></ul>
    72. Predicting Maintenance of Cognition <ul><li>What activity best combines all predictive factors -------------SHOPPING </li></ul>
    73. Overview of Recent Progress Hope for Tomorrow <ul><li>Genetics Provides Clues for Drug Development </li></ul><ul><li>Clinical Research Emphasizes Importance of Early Diagnosis </li></ul><ul><li>Technology Provides Methods for Tracking Evolution of Disease </li></ul><ul><li>Population Studies Provide Clues to Factors that Promote Brain Health </li></ul>
    74. Summary - Epochs of Progress <ul><li>100 years ago – unknown as a disease </li></ul><ul><li>25 years ago – no research effort </li></ul><ul><li>15 years ago – no known genes associated with AD, limited understanding of biological pathways </li></ul><ul><li>10 years ago – no animal models of disease </li></ul><ul><li>5 years ago – no prevention trials funded, limited ability to identify persons at high risk, limited knowledge about factors that promote brain health </li></ul>
    75. Strategy that Maximized Progress <ul><li>Identification of research areas that required improved funding </li></ul><ul><li>Recruitment of outstanding scientists into field </li></ul><ul><li>Communication to Government regarding importance of problem: No Time To Lose – Invest in Research </li></ul><ul><li>Speaking with One Voice regarding strategy </li></ul>

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