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Biennial Report of the Director
National Institutes of Health Fiscal Years 2008 & 2009

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Biennial Report of the Director

NIH Centers of Excellence
Alzheimer's Disease Centers









Overview

Why the ADCs Were Established

In 1984, Congress directed NIH to foster further research related to Alzheimer's disease (AD). The Public Health Service Act authorizes the NIH Alzheimer’s Disease Centers (ADCs) program under section 445 (42 U.S.C. 285e-2). NIH funded the first ADCs in the mid-1980s in response to the congressional directive, information on AD emerging from the work of NIH grantees and other researchers, and the prospect of a medical and social crisis triggered by an explosion of AD cases as the population ages. The principal objectives of the ADC program are to promote research, research, training, outreach, and technology transfer. Much of the research takes place through multicenter cooperative studies to better understand the causes and effects of AD and to develop and test new interventions for the diagnosis, treatment, and prevention of AD and other age-related neurodegenerative diseases (diseases in which the cells of the brain and spinal cord are lost) and normal aging.


How the ADCs Function Within the NIH Framework

NIH currently funds 30 ADCs (see Table 4-1). Funding for the ADCs comes from NIA through the P30 (center core grant) and P50 (specialized center grant) mechanisms for 5 years and then must compete through a peer review process for additional funding. New applicants for ADCs compete with existing grantees. If existing centers are unsuccessful in competition, new centers are funded to take their places.

NIH currently funds 30 Alzheimer’s Disease Centers through a congressionally mandated program initiated in 1984.

Description of Disease or Condition

AD is the most common form of dementia among older people. It is an age-related, irreversible brain disorder that develops over many years. In the very early stage, people experience memory loss, which can be mistaken for memory changes that occur in normal aging. As the disease progresses, these symptoms gradually lead to dementia, a condition characterized by marked memory loss and behavior and personality changes. The disease also leads to a decline in other cognitive abilities (such as decision-making and language skills) and, eventually, an inability to recognize family and friends and a severe loss of mental function. These losses are related to the breakdown of the connections between neurons (nerve cells) in the brain and to the eventual death of many of these cells. In most people, symptoms first appear after age 60. AD and other dementing disorders are caused by disease processes that affect the brain, although age-related brain and body changes also can affect the development of AD and other dementias.

AD is named after Dr. Alois Alzheimer, a German doctor who, more than 100 years ago, studied the brain tissue of a woman who had died of an unexplained mental illness. Dr. Alzheimer found unusual features of her brain tissue—many deposits of sticky proteins in the spaces between neurons, now known as beta-amyloid plaques, and tangled bundles of fibrils (thin fibers) within neurons, now known as neurofibrillary tangles. However, it was not until the 1960s and 1970s that scientists began to recognize AD as a disease associated with aging.1 Today, plaques and tangles in the brain are considered signs of AD, as are other brain changes, including the death of neurons in areas of the brain that are vital to memory and other mental abilities and the disruption of connections, called synapses, that allow neurons to communicate with each other. The disease also is characterized by low levels of some of the chemicals in the brain that carry messages between neurons. AD impairs thinking and memory by disrupting these messages.

Scientists are finding evidence that some of the risk factors for heart disease and stroke—such as high blood pressure, high cholesterol, and low levels of the vitamin folate—might increase the risk for AD. Evidence also is increasing that physical, mental, and social activities may protect people from AD.

AD probably has no single cause. The most important known risk factors are age and family history, although education, diet, and environment also might play a role. Scientists also are finding evidence that some of the risk factors for heart disease and stroke—such as high blood pressure, high cholesterol, and low levels of the vitamin folate—might increase the risk for AD. Evidence also is increasing that physical, mental, and social activities may protect people from AD. Although scientists have learned a great deal about AD, they still do not know what causes the disease and have not identified a cure.


1 Katzman R. Arch Neurol 1976;33(4):217-8. PMID: 1259639.


Burden of Illness

Recent estimates from a nationally representative sample in the Aging, Demographics, and Memory Study (part of the ongoing NIH-supported Health and Retirement Study) suggest that one in seven Americans age 72 or older has dementia and about 2.4 million have AD.2 Other investigators, using projections from community-based studies, estimate that 5.1 million Americans ages 65 or older will have AD in 2010.3 Despite the differing methodologies and results of their studies, experts agree that the number of people with AD will increase significantly if current U.S. population trends continue and no prevention methods emerge. Our aging society makes AD an especially critical issue because the number of people with the disease doubles for every 5-year age interval beyond age 65. The U.S. Census Bureau estimates that the size of the population ages 65 and older will double to about 72 million people in the next 25 years. Moreover, the fastest growing segment of the U.S. population is comprised of people 85 years of age or older.


2 Hebert LE, et al. Arch Neurol 2003;60:1119-22. PMID: 12925369.
3 Hebert LE, et al. Arch Neurol 2003;60:1119-22. PMID: 12925369.


Scope of NIH Activities: Research and Programmatic

The ADC program provides infrastructure and core resources to enhance ongoing research by bringing together basic biomedical, behavioral, and clinical scientists to study the causes, progression, prevention, diagnosis, and treatment of AD and to improve health care delivery. ADCs also foster the development of new research approaches and provide suitable environments for research fellows and junior faculty to acquire the necessary skills and experience for interdisciplinary AD research.

NIH requires all 30 ADCs to have the following cores: administrative, clinical, data management and statistics, education and information transfer, and neuropathology. Some centers include other optional cores, such as neuroimaging or genetics cores, and some have satellite diagnostic and treatment clinics to help recruit minority or rural research participants.

The ADC program comprises two types of centers. Alzheimer’s Disease Research Centers conduct research projects in addition to providing core resources. The Alzheimer’s Disease Core Centers consist of cores only and provide investigators with access to well-characterized patients, patient and family information, and tissue and other biological specimens for use in separately funded research projects.

By pooling resources and working cooperatively with other ADCs, these centers have produced research findings and developed resources that individual investigators working alone could not have achieved.

By pooling resources and working cooperatively with other ADCs, these centers have produced research findings and developed resources that individual investigators working alone could not have achieved. ADCs have provided biological samples from patients with AD for hundreds of non-ADC funded projects. Several major long-term studies on the development of dementia in specific populations rely on ADC core facilities and integrate their findings with those of the centers.

Examples of resources shared among ADCs are the brain and specimen banks at each center, which consist of well-characterized specimens collected under standardized protocols. Another resource shared by the ADCs is the National Cell Repository for Alzheimer’s Disease (NCRAD) at Indiana University, which collects and stores blood, DNA, and cell lines from families with several affected members and from unaffected control participants. NCRAD also stores well-documented phenotypic data, which includes the observable traits or characteristics of a person, such as age and gender, as well as the presence or absence of a disease. The repository is part of the NIH Alzheimer’s Disease Genetics Initiative, which was established to identify genetic risk factors for late-onset AD, and the recently funded Alzheimer’s Disease Genetics Consortium, which conducts large-scale whole-genome studies on AD.

The ADCs have helped create additional collaborative research resources or projects, such as the Consortium to Establish a Registry for Alzheimer's Disease, the National Alzheimer’s Coordinating Center, the Alzheimer’s Disease Cooperative Study, and the Alzheimer’s Disease Neuroimaging Initiative. Descriptions of these and other efforts are provided below.

Much important progress in AD research in the United States during the past 25 years stems from research conducted at the ADCs, as well as from resources and infrastructure provided by the centers. Through ADC research, scientists have identified mutant genes on three chromosomes whose presence could result in the rare early-onset, inherited AD; discovered a version of a gene on chromosome 19 that is a risk factor for the more common late-onset AD; and determined that mutant genes on chromosome 17 are associated with frontotemporal dementia, a group of rare dementia disorders that affect the parts of the brain that are associated with language and behavior. Other studies have revealed the importance of the abnormal processing of proteins encoded by these genes.

Through ADC research, scientists have identified mutant genes on three chromosomes whose presence could result in the rare early-onset, inherited AD and discovered a version of a gene on chromosome 19 that is a risk factor for the more common late-onset AD.

ADC scientists have conducted much of the research on protein processing related to plaque and tangle formation, including the discovery of a protein implicated in the development of Lewy body dementia (which can cause confusion, rigid muscles, slower movement, and tremors). ADC researchers also identified the common properties of the abnormal proteins associated with several neurodegenerative diseases, which are characterized by damage or loss of neurons in the brain and spinal cord. Additional support through ARRA funding to the Johns Hopkins ADC will enhance research efforts in studies of brain pathology.

In recent years, ADC researchers have evaluated cognitive changes associated with normal aging and the transitions to mild cognitive impairment (early difficulties with thinking and remembering) and dementia. They also have identified factors that contribute to changes in cognitive abilities.

Currently, many ADCs are carrying out important studies relating changes in brain structure to different clinical stages of AD. For these studies, researchers are examining patients enrolled in the clinical cores, brain imaging supported by imaging cores, and autopsy evaluations in neuropathology cores. ADC researchers  also are examining relationships and commonalities between AD and cerebrovascular disease or other neurodegenerative diseases as well as contributions of co-existing non-neurological conditions that occur in people with AD.

The ADCs are exploring commonalities between AD and other dementias that involve Lewy bodies and between AD and Parkinson’s disease dementia. In this regard, collaborations are underway with the NINDS-supported Udall Parkinson’s Disease Centers to examine the overlapping scientific and clinical issues.

Many (18) ADCs also participate in the NIH Late Onset Alzheimer’s Disease (LOAD) Genetics Initiative, which was launched to help advance AD-related genetics research. LOAD aims to collect samples from more than 1,000 families having at least two members with late-onset AD as well as 1,000 control participants. The Columbia University AD Research Center serves as the coordination center for LOAD. To complete enrollment, characterization, and follow-up of patients and control participants in the LOAD Genetics Initiative, NIH awarded a resource grant to a consortium of six ADCs. As of 2009, more than 5,000 new blood samples from approximately 800 late-onset AD families have been sent to the National Cell Repository for Alzheimer’s Disease, another important resource for the ADCs. In a search for risk factor genes, ADC researchers are analyzing data derived from whole-genome scans of LOAD samples.

The ADCs are contributing phenotypic information and DNA specimens from participants enrolled in ADC studies to a major new genomic project carried out by the NIH-funded Alzheimer’s Disease Genetics Consortium, which will perform whole-genome scans using specimens from up to 10,000 human subjects enrolled in the ADCs as well as from other major population studies.

The ADCs also are contributing phenotypic information and DNA specimens from participants enrolled in ADC studies to a major new genomic project carried out by the NIH-funded Alzheimer’s Disease Genetics Consortium (ADGC). The ADGC will perform whole-genome scans using specimens from up to 10,000 human subjects enrolled in the ADCs as well as from other major population studies. In FY 2009, ARRA funds were awarded to the ADGC to add 3,800 AD patients and an equal number of people free of disease, thus making this one of the largest collections of samples available for genome-wide association studies in an effort to identify the susceptibility and protective genes influencing the onset and progression of late-onset disease.

Another major objective for the ADCs is to recruit minority and ethnically diverse research participants for AD research. To achieve this goal, NIH created the Satellite Diagnostic and Treatment Clinics and linked them to the ADCs. The number of satellites has fluctuated; 23 currently are active and are recruiting African American, Hispanic, Native American, and Asian research participants. National Alzheimer’s Coordinating Center data now show that approximately 20 percent of those enrolled in the ADCs are minorities. Also, the ADCs conduct research related to minority concerns in cooperation with the NIH-supported Research Centers on Minority Aging Research. In addition, ARRA funds were awarded to two ADCs to help understand the factors that affect recruitment of minority populations in their studies. These two supplements will be used to study recruitment of African American participants at a satellite clinic at the University of Kentucky’s ADC and at the Boston University ADC.

National Alzheimer’s Coordinating Center data now show that approximately 20 percent of those enrolled in the ADCs are minorities.

All ADCs have Education and Information Transfer Cores (EITCs) that provide research training for new investigators, as well as outreach to the public, including caregivers. EITC efforts also have been redefined recently to facilitate participant recruitment for projects such as the NIA Genetics Initiative, Alzheimer’s Disease Cooperative Study, Alzheimer’s Disease Neuroimaging Initiative, and other clinical trials and initiatives. Collaborations include ongoing interactions with groups such as the Alzheimer’s Association and NIH’s Alzheimer’s Disease Education and Referral Center. The ADCs pay special attention to cultural sensitivity and, where appropriate, structure their information to effectively reach minority populations, including non-English-speaking people.

The three New York City ADCs—at Columbia University, Mount Sinai School of Medicine, and New York University—and the New York City chapter of the Alzheimer’s Association jointly formed the New York Consortium for Alzheimer’s Research and Education in 2000. The consortium provides continuing medical education programs for community physicians on AD diagnosis, management, and research opportunities.


NIH Funding for FY 2008 and FY 2009

Actual NIH funding for the ADCs was $51.0 million in FY 2008 and $51.9 million in FY 2009, including $0.7 million from ARRA funds.


FY 2008 and FY 2009 Progress Report

Programmatic Activities and Outcomes

Programmatic accomplishments for the ADCs include the following examples.

  • National Alzheimer's Coordinating Center (NACC): In 1999, NIH established NACC to facilitate collaborative research and standardize procedures among the ADCs. NACC developed and maintains a large database of standardized clinical and neuropathological research data collected from each ADC. This database provides a valuable resource to qualified research scientists for both exploratory and explanatory AD research. The data provided by NACC support large studies that use patient samples from diverse populations and multiple ADCs. NACC collects standardized data (the Uniform Data Set or UDS) collected over time from research participants who are examined annually.

    Currently, the ADCs are following about 15,000 research participants, and NACC is storing these data. NACC has adopted new procedures for widening access to the database by non-center scientists. NACC has funded 18 collaborative multicenter studies using its own resources, and an additional 8 NIH-funded collaborative research project R01 grants are linked to NACC.

  • Alzheimer’s Disease Cooperative Study (ADCS): All of the ADCs are performance sites for the ADCS, which is the cornerstone of NIH’s major AD clinical trials effort. ADCS is a large clinical trials consortium that expanded from the ADCs and now includes sites throughout the United States and Canada. The clinical research outcomes of ADCs are inextricable from the outcomes of ADCS.

    NIH developed the ADCS to advance research on drugs that might be useful for treating patients with AD, particularly drugs that industry might not develop. The study tests agents that lack patent protection; drugs that are under patent protection but marketed by manufacturers for other diseases; and novel compounds developed by individuals, academic institutions, and small biotechnology companies. The ADCS also develops new evaluation instruments for clinical trials, as well as novel approaches to clinical trial design.

    Since its inception, the ADCS has initiated 30 research studies, 23 drug trials, and 7 instrument-development protocols. Studies currently underway at ADC performance sites include:
    • A trial examining whether treatment with docosahexaenoic acid, an omega-3 fatty acid, will slow decline in AD.
    • A trial evaluating the efficacy and safety of intravenous immunoglobulin, which contains naturally occurring antibodies against beta-amyloid, in patients with mild-to-moderate AD.
    • A multicenter trial evaluating home-based assessment methods for AD prevention research in people ages 75 and older.

  • Alzheimer’s Disease Neuroimaging Initiative (ADNI): Most ADCs participate in ADNI, which is an innovative public-private partnership that is examining the potential of serial magnetic resonance imaging (MRI), positron emission tomography (PET), or biomarkers to measure earlier, and with greater sensitivity, the development and progression of mild cognitive impairment and AD. As is true of the ADCS, the activities and outcomes of ADNI are inextricable from those of the ADCs. ADNI completed enrollment in August 2007 and now is monitoring the 823 participants using MRI and PET imaging and laboratory and cognitive tests. This will generate a comprehensive database that will serve as an important public resource to spur further research. Already, many of the tools and methods developed by the study are fueling similar efforts in Japan, the European Union, and Australia.

    In 2007, ADNI obtained additional funds to conduct a genome-wide association study (GWAS) and analyze the genetic variations among ADNI participants. This effort will provide the most extensive and robust dataset of its kind in AD research and will be a critical resource for ADC investigators among others. Supplemental funding from NIH allows the collection of cerebrospinal fluid from participants, while funding from a third NIH supplement is used to explore the use of PET imaging and Pittsburgh compound B (PiB, an amyloid imaging agent) as tools for developing biochemical and imaging markers.

    Results from an ADNI study confirmed that certain changes in biomarker levels in cerebrospinal fluid might signal the onset of mild AD and established methods and standards for testing these biomarkers (see “Research Accomplishments” for more details). More than 1,000 researchers, as well as other interested individuals, already have accessed a public database containing thousands of brain images, related clinical data, and blood and cerebrospinal fluid analyses.

    In FY 2009, ARRA funds were awarded to ADNI to expand the scope of ongoing research by allowing for the enrollment of participants at an earlier stage of mild cognitive impairment (MCI), when symptoms are milder. Furthermore, the funding for this new grant will allow ADNI investigators to extend the length of the original study to better assess changes in individuals over time. The overall impact of the added funding will be increased knowledge of the sequence and timing of events leading to MCI and Alzheimer’s disease and development of better clinical and imaging/fluid biomarker methods for early detection and for monitoring the progression of these conditions. This will facilitate clinical trials of treatments to slow disease progression and ultimately will contribute to the prevention of Alzheimer’s disease.


Research Activities and Outcomes

Since the establishment of the ADC program in 1984, investigators have published thousands of research papers on all aspects of AD and related disorders. Topics have ranged from the disease’s biology to its family and societal impact, as well as many studies of diagnosis and treatment.

Research accomplishments include the following important recent studies carried out by ADC scientists, which highlight research on biomarkers and AD recently carried out by several centers. These studies are only a few examples from a wide spectrum of research studies conducted by the ADCs.

  • Beta Amyloid Deposition Imaging.4 The progressive accumulation of a protein called beta amyloid in the brain is a hallmark of AD. Previously, a researcher’s ability to measure the amount of beta amyloid in a person’s brain could only be accomplished at autopsy. Now, with the development of the new tracer element PiB (Pittsburgh Compound B), researchers can visualize the amount of beta amyloid in the brains of living people. Investigators at the University of Pittsburgh ADC studied PiB binding in the brain using PET imaging to visualize beta amyloid in the brains of living people over age 65. The participants did not have symptoms of AD or other less severe forms of dementia, such as mild cognitive impairment. Of the brains imaged, 21 percent showed evidence of early amyloid deposition in at least one brain area. Demographic characteristics such as gender did not differ significantly between those with and without beta amyloid in their brains. Importantly, the researchers were able to demonstrate that beta amyloid can be identified in the brains of cognitively normal older persons during life and that some older persons can remain cognitively normal despite a significant amount of beta amyloid within their brains. Further studies over a longer period of time now are necessary to ascertain the potential of PiB imaging to identify preclinical AD or, alternatively, to show that beta amyloid deposition alone is not sufficient to predict AD in the future.
Previously, a researcher’s ability to measure the amount of beta amyloid in a person’s brain could only be accomplished at autopsy. Now, with the development of the new tracer element PiB (Pittsburgh Compound B), researchers can visualize the amount of beta amyloid in the brains of living people.
  • Biomarkers of Presymptomatic AD.5 For AD treatments to have the greatest impact, health care providers will need to treat individuals before symptoms appear. Investigators are exploring fluid and neuroimaging measures as possible biomarkers of AD pathology that could aid in identifying individuals during the earliest stages of their disease to direct and monitor therapy. For example, researchers at the Washington University ADC investigated the relationship between brain volume (as measured by MRI) and an array of proteins that are implicated in the eventual development of AD in cognitively normal participants and individuals who have been diagnosed with early AD. They recently found that lower levels of the toxic protein fragment amyloid beta-42 in cerebrospinal fluid (CSF)—a colorless fluid that circulates through and around the central nervous system, including the brain—in cognitively normal people appear to be associated with lower brain volume, suggesting some damage to the brain. The study indicates that increases in the protein tau take place later in the course of the disease and are more closely associated with clinical onset and progression of AD. Taken together, these results provide additional evidence that amyloid-associated brain damage may occur well before clinical symptoms appear.
  • Cerebrospinal Fluid Biomarkers.6 In the first ADNI CSF biomarker study, NIH-supported researchers, including ADC researchers, established a method and standard for testing levels of two candidate biomarkers for AD—tau and beta amyloid proteins, which are potential biomarkers for AD in the brain and the CSF. The researchers now have correlated levels of these proteins in CSF with changes in cognition over time and determined that changes in these two protein levels in CSF may signal the onset of mild AD. This is a significant step forward in developing a test to help diagnose the early stages of AD sooner and more accurately to begin treatment that could delay the development of more severe AD symptoms. In fact, this effort may open the door to the discovery of an entire panel of CSF biomarkers that will not only identify people at risk of developing AD, but also assess how the disease responds to therapies. Importantly, these data are available online to qualified researchers worldwide.
Researchers have correlated levels of two proteins in cerebrospinal fluid with changes in cognition over time and determined that changes in these two protein levels may signal the onset of mild AD.
  • Measuring the Effects of AD Treatment.7 Recently, ADC investigators used a new method of stable isotope labeling in which they “tagged” molecules in a compound with a radioactive tracer to assess the effects of an experimental drug on the production and clearance rates of proteins that are implicated in the development of AD and other central nervous system (CNS) disorders. The results from this approach might help investigators make decisions about drug effectiveness and dosing in designing larger and longer clinical trials for diseases such as AD and may accelerate effective drug validation. Notably, this is the first time that investigators have been able to measure directly over time the reduction of beta amyloid in CSF by a drug that typically inhibits its production. This approach provides a means for testing the relative effects of dose and drug in current and novel therapeutic agents.

 


4 Aizenstein HJ, et al. Arch Neurol 2008;65(11):1509-17. PMID: 19001171. PMCID: PMC2636844.
5 Aizenstein HJ, et al. Arch Neurol 2008;65:1509-17. PMID: 19001171. PMCID: PMC2636844.
6 Shaw LM, et al, Ann Neurol 2009;65(4):403-13, PMID: 19296504. PMCID: PMC2696350.
7 Bateman RJ, et al. Ann Neurol 2009;66(1):48-54, PMID: 19360898. PMCID: PMC2730994.


Recommendations for Improving the Effectiveness, Efficiency, and Outcomes of the ADCs

Since their launch in 1984, the NIH ADCs have continued to grow, and many multicenter initiatives have begun. In 2008, the National Advisory Council on Aging, an external advisory committee, reviewed the program’s progress in achieving recommendations made in 2002. The council suggested that NIH examine the need to revise clinical diagnostic criteria for AD for identifying people with AD at an earlier stage in its development so that clinicians can prescribe strategies for delaying the onset of AD. That initiative is currently underway.


Evaluation Plans

The National Advisory Council on Aging evaluates and makes recommendations for the ADC program every 4 years. The next evaluation will be in 2012.


Future Directions

NIH plans for the ADCs to continue to place less emphasis on late-stage AD and will concentrate instead on the transition from normal aging to mild cognitive impairment and to full-blown AD, as well as on studies of the overlap between AD and other neurodegenerative diseases. In addition, the ADCs will continue to search for biomarkers that predict cognitive decline and diagnose cognitive impairment and dementia. NIH will continue to support existing ADCs, which must recompete for funding after each grant cycle (typically every 5 years) and award new grants to institutions that the NIH peer-review process deems to be qualified.


Table 4-1. Alzheimer's Disease Centers of Excellence (ADCs)
Institution and Location Year Established
University of California, San Diego, CA 1984
Massachusetts General Hospital, Boston, MA 1984
Mount Sinai School of Medicine, New York, NY 1984
University of Southern California, Los Angeles, CA 1984
Johns Hopkins University, Baltimore, MD 1984
Duke University, Durham, NC 1985
University of Kentucky, Lexington, KY 1985
University of Pittsburgh, Pittsburgh, PA 1985
University of Washington, Seattle, WA 1985
Washington University in St. Louis, MO 1985
University of Texas Southwestern Medical Center, Dallas, TX 1988
University of Michigan, Ann Arbor, MI 1989
Columbia University Health Sciences, New York, NY 1989
Oregon Health & Science University, Portland, OR 1990
New York University School of Medicine, New York, NY 1990
Mayo Clinic College of Medicine, Rochester, NY 1990
University of Pennsylvania, Philadelphia, PA 1991
University of California Davis School of Medicine, Sacramento, CA 1991
Indiana University‐Purdue University, Indianapolis, IN 1991
Rush University Medical Center, Chicago, IL 1991
University of California, Los Angeles, CA 1991
Boston University Medical Campus, Boston, MA 1996
Northwestern University, Chicago, IL 1996
University of Alabama, Birmingham, AL 1999
University of California, Irvine, CA 2000
Arizona Alzheimer’s Center, Phoenix, AZ 2001
University of California, San Francisco, CA 2004
Emory University, Atlanta, GA 2005
Florida Alzheimer’s Center, Tampa, FL 2005
University of Wisconsin, Madison, WI 2009