UAB Synopsis, Vol. 26, No. 29, August 6, 2007
The UAB Alzheimer’s Disease Center (ADC), an interdisciplinary, university-wide center in the Department of Neurology, was established in 1991 to coordinate diagnosis, treatment, research, and education about a disease that its new director anticipates will grow to tidal wave proportions in coming decades as Americans age .
Daniel C. Marson, JD, PhD, named director in April, expects the ADC to play a significant role in a national effort to “bring down that tidal wave through research aimed at understanding, altering, and ultimately preventing the disease course.”
Dr. Marson, who joined the center in 1991 and served as interim director since October 2005, sees a strengthened basic research component as key to efforts to intervene earlier in the disease process, delay or prevent symptoms, and eventually cure the disease. He also is directing more resources into higher risk groups, especially African Americans, and sees a natural confluence of research activities with other neurodegenerative diseases, such as Parkinson’s disease (PD).
Dr. Marson estimates that by 2050 as many as 13.2 million individuals in the United States will be living with AD. “This will place a tremendous burden on both families and government resources, so our challenge is great,” he says.
The ADC holds multiple federal and industry research awards and since 1999 has been a federal Alzheimer’s Disease Research Center (ADRC) — 1 of 32 such units currently funded by the National Institute on Aging (NIA). The NIA grant is organized around five cores.
An Administrative Core, led by Dr. Marson, provides organizational, fiscal, and procedural management for the ADC as a whole. A Clinical Core recruits and follows four participant groups longitudinally to study neurologic, cognitive, psychiatric, and everyday functional changes. These groups of interest are: patients with mild cognitive impairment (MCI), patients with mild AD, patients with PD and dementia, and a control group of normal, older individuals. Neuropsychologist H. Randall Griffith, MD, is interim director and geriatric psychiatrist and neuropathologist Richard E. Powers, MD, is interim assistant director.
Neurology instructor and social worker J. Miller Piggott, who also is executive director of Alzheimer’s of Central Alabama, the state’s major AD caregiver group, directs an Education and Information Transfer Core.
A Neuropathology Core, directed by neuropathologist Steven L. Carroll, MD, focuses on obtaining and distributing autopsy-based brain tissue for investigators.
A Biostatistics Core directed by Alfred A. Bartolucci, PhD, provides data management and analytic services to the ADC.
African American Outreach
By 2030 an estimated 7 million African Americans will enter the age of risk for developing Alzheimer’s disease. “We established a Minority Outreach Advisory Board in October 2006, and with its assistance are building bridges within the community to better educate family members to recognize early signs of Alzheimer’s and seek early diagnosis and treatment,” Dr. Marson says. Dr. Powers directs the Harper Project, a collaboration with historically black colleges in Alabama that includes faculty exchanges and mentored fellowships, currently through Miles College in Birmingham and Alabama A&M University in Huntsville.
Research Activities
“The ADC in the past has been very clinically oriented, and we have gained recognition as a major resource in Alabama and our region for diagnosis and treatment of Alzheimer’s disease. We now are striving to achieve greater balance between basic and clinical studies,” Dr. Marson says. The research portfolio includes an emphasis on a better understanding of issues in African Americans, such as the role of cerebrovascular factors, and how MCI in that population may differ across racial groups. A minority recruitment specialist, Sharonda Hardy, joined the ADRC in July 2006 to assist in recruitment and community outreach.
Cross-dementia studies between AD and PD comprise a second research focus. “With the arrival of eminent Parkinson’s researcher Dr. Ray L. Watts to chair the Department of Neurology, and the more recent appointment of Dr. David G. Standaert as director of the Center for Neurodegeneration and Experimental Therapeutics, we are well positioned to compare the dementias of Parkinson’s-spectrum disorders with AD,” he says. A number of studies comparing particular functional changes in AD and PD are already underway. “As both the AD and PD programs grow, I think they will link together very effectively.”
A third area of research involves mouse models of AD, a significant interest of J. David Sweatt, PhD, who arrived last year to chair the Department of Neurobiology.
Looming Crisis, Recent Progress
“We’ve seen tremendous progress on AD in the last 30 years because of NIA’s recognition of the urgent need for effective treatments and ultimately a cure. An important step to address the challenge will be to find treatments that can delay disease onset by 5 to 10 years,” he says.
Dr. Marson says scientists are well along the path to understanding disease mechanisms — the biology of brain pathology that includes senile plaques and neurofibrillary tangles. Scientists have made strides in development of mouse models of AD, and initial work on vaccines has begun. Neuroimaging has developed to the point of accurately displaying amyloid distribution and load in the brain. In addition, investigators are beginning to identify new genetic components of AD.
Dr. Marson’s optimism is bolstered by a sense of joint collaboration that pervades the field of AD research, which he says is reflected in the NIA’s development of the Alzheimer’s Disease Cooperative Study, a consortium of AD centers nationwide that carry out clinical trials, and also the national collaborative Alzheimer’s Disease Neuroimaging Initiative. The UAB ADC participates in both studies. “These large collaborative studies are the direction we need to go, because the issues are so important and because we require large data sets to answer key questions.
“We now have first-generation drugs, but only for short-term treatment of AD symptoms,” Dr. Marson says. “It’s clear that we need to alter the course of the disease because by the time AD or MCI is diagnosed, the brain already has suffered substantial damage. We want to identify the disease process earlier and intervene before it substantially affects the brain. I am optimistic that we will find ways to identify and modify the biological pro-cesses that ultimately cause the dementia we know as AD.”
The ADC is housed in newly renovated offices on the sixth floor of the Sparks Clinic. Dr. Marson is available at 205.934.2335 or dmarson@uab.edu.