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WAI Faculty & Staff

Mark Sager, MD, Director


Contact Information

Phone: 608-829-3300
Mailing address: Wisconsin Alzheimer's Institute, UW School of Medicine and Public Health, 7818 Big Sky Drive, Suite 215, Madison, WI 53719


Director, Wisconsin Alzheimer's Institute, University of Wisconsin School of Medicine and Public Health; Professor of Medicine, Departments of Medicine and Population Health Sciences, University of Wisconsin, Madison; Associate Director, Wisconsin Alzheimer's Disease Research Center, University of Wisconsin School of Medicine and Public Health



B.S., 1968 Chemistry and Biology, University of Illinois (Champaign); M.D., 1972 University of Michigan; Residency, 1972-1975, Internal Medicine, University of Minnesota; 1985-1987, Geriatrics Fellowship, University of Wisconsin-Madison



Phi Beta Kappa, Phi Kappa Phi, Alpha Omega Alpha (medicine)


Research Interests

Alzheimer's disease prevention; Improving quality of care in long term care



Dr. Sager is Director of the Wisconsin Alzheimer's Institute and a Professor of Medicine at the University of Wisconsin-Madison School of Medicine and Public Health. He is the founder of the Wisconsin Registry for Alzheimer's Prevention (WRAP) which is a longitudinal study of adult children of persons with Alzheimer's disease. The primary goal of WRAP is to conduct genetic, epidemiological and clinical research that could lead to the prevention of Alzheimer's disease. Dr. Sager also developed the WAI affiliated network of dementia diagnostic clinics consisting of Wisconsin physicians and health care providers dedicated to improving the care provided to persons with Alzheimer's disease and their families. He is a fellowship trained geriatrician and received his MD from the University of Michigan. Dr. Sager joined the UW faculty in 1992.


Research Description

The proportion of the population aged 65 and older is projected to increase from 13% in 2000 to 20% by 2030, primarily because of the aging of the baby boom generation and increased longevity. Persons aged 85 and older (the oldest old) will represent an increasing proportion of this aging population and an estimated 40% of persons turning 65 in 2000 will survive to the age of 85 years. The implications of this aging phenomenon for the delivery and financing of long-term care will be especially profound because the oldest old are the largest consumers of long-term care services and one-half of them will develop Alzheimer's disease.


Alzheimer's disease currently affects between 5-10% of the population aged 65 and older and is the most frequent cause of institutionalization for long-term care in the United States. An estimated $2 billion of public and private dollars is spent each year in Wisconsin for nursing home care alone, and almost half of that is to provide care for persons suffering from Alzheimer's disease and related dementias. In Wisconsin, the number of affected persons is expected to increase by 58% from 103,000 to 163,000 persons over the next 25 years. The expected rapid increase in the number of persons with Alzheimer's disease will translate into higher public and private long-term care costs that will be paid by private payers, state Medicaid programs and long-term care insurers. One way to reduce the cost of long-term care is to lower the need for long-term care by delaying the onset or slowing the progression of Alzheimer's disease. Estimates are that a delay in the onset of Alzheimer's disease by five years would result in a 50% reduction in prevalence in one generation. A 10-year delay in the onset of Alzheimer's disease would result in only 3.5 million affected persons by 2040 instead of the anticipated 14 million persons.


Current data indicate that Alzheimer's disease is a lifelong disease with a prolonged pre-clinical phase during which prevention strategies would be most effective in delaying or preventing the onset of Alzheimer's disease. Neuritic plaques and neurofibrillary tangles, the pathological hallmarks of Alzheimer's disease, have been found in adults without dementia, suggesting that the neuronal deficits leading to Alzheimer's disease begin years before any symptoms develop. Other studies have found metabolic and structural changes, typical for Alzheimer's disease, in the brains of asymptomatic middle aged persons. As in other chronic degenerative diseases of aging, a person's risk of developing symptoms of Alzheimer's disease is most likely the result of genetic, environmental, socioeconomic and lifestyle factors which interact to determine age of onset. Because of this, a person's risk of developing symptoms of Alzheimer's disease is potentially modifiable either by changes in the environment or lifestyle or through external interventions.

Dr. Sager's research interests are in identifying ways to delay the onset or slow the progression of Alzheimer's disease using the latest knowledge and technologies available. He is also committed to developing programs that promote: early diagnosis and treatment of persons with Alzheimer's disease; improved quality of care for persons with Alzheimer's disease; and recognition of the unique needs of families and caregivers of persons with Alzheimer's disease.


Representative Publications (2005 to present)

Woodard JL, Dorsett E, Cooper JG, Hermann BP, Sager MA. Development of a brief cognitive screen for mild cognitive impairment and neurocognitive disorder. Aging Neuropsychol Cog 2005; 12(4):299-315.


Ward MA, Carlsson CM, Trivedi MA, Sager MA, Johnson SC. The effect of body mass index on global brain volume in middle-aged adults: a cross-sectional study. BMC Neurology 2005; 5:23.


Sager MA, Hermann BP, La Rue A. Middle-aged children of persons with Alzheimer's disease: APOE genotypes and cognitive function in the Wisconsin Registry for Alzheimer's Prevention. J Geriatr Psychiatry Neurol 2006; 18:1-5.


Sager MA, Johnson SC. Commentary on "Perspective on a pathogenesis and treatment of Alzheimer's disease." Comment on the mitochondrial metabolism hypothesis. Alzheimer's and Dementia 2006; 2(2):74-75.


Trivedi MA, Schmitz TW, Ries ML, Torgerson BM, Sager MA, Hermann BP, Asthana S, Johnson SC. Reduced hippocampal activation during episodic encoding in middle-aged individuals at genetic risk of Alzheimer's disease: a cross-sectional study. BMC Medicine 2006; 4:1.


Johnson SC, Schmitz TW, Trivedi MA, Ries ML, Torgerson BM, Carlsson CM, Asthana S, Hermann BP, Sager MA. The influence of AD family history and APOE-4 on mesial temporal lobe activation. J Neuroscience 2006; 26(22):6069-6076.


Sager MA, Hermann BP, La Rue A, Woodard JL. Screening for dementia in community-based memory clinics. Wisconsin Medical Journal 2006; 105(7):23-27.


Thal L, Kuller L, Bowman K, Breitner J, Evans D, Farrer L, Frank R, Khachaturian AS, Khachaturian ZS, Kukull W, Nieto J, Petersen R, Sager MA, Scherr P, Bain LJ. The Nevada Vital Aging Initiative: a private-public partnership to study early predictions of dementia. Alzheimer's and Dementia 2007; 3(1):62-67.


Johnson SC, Ries ML, Hess TM, Carlsson CM, Gleason CE, Alexander AL, Rowley HA, Asthana S, Sager MA. Alzheimer's disease risk in healthy middle-aged adults affects brain function during self-appraisal. Arch Gen Psychiatry 2007; 64(10)1163-1171.


Carlsson CM, Gleason CE, Hess TM, Moreland KA, Blazel HM, Koscik RL, Schreiber NT, Johnson SC, Atwood CS, Puglielli L, Hermann BP, McBride PE, Stein JH, Sager MA, Asthana S. Effects of simvastatin on cerebrospinal fluid biomarkers and cognition in middle-aged adults at risk for Alzheimer's disease. J Alzheimers Dis 2008; 13:187-197.


La Rue A, Hermann BP, Jones JE, Johnson SC, Asthana S, Sager MA. Effect of parental family history of Alzheimer's disease on serial position profiles. Alzheimer's and Dementia 2008; 4:285-290.


Carlsson CM, Nondahl DM, Klein BEK, McBride PE, Sager MA, Schubert C, Klein R, Cruickshanks KJ. Increased atherogenic lipoproteins are associated with cognitive impairment: effects of statins and sub-clinical atherosclerosis. Alz Dis Assoc Disord 2009; 23:11-17.


Xu G, McLaren DG, Ries ML, Fitzgerald ME, Bendlin BB, Rowley HA, Sager MA, Atwood C, Asthana S, Johnson SC. The influence of parental history of Alzheimer's disease and apolipoprotein E e4 on the BOLD signal during recognition memory. Brain 2009; 132(2):383-391.


Weimer DL, Sager MA. Early identification and treatment of Alzheimer's disease: social and fiscal outcomes. Alzheimer's and Dementia 2009; 5(3):215-226.


Sager MA, Hermann BP, La Rue A. Middle-aged children of persons with Alzheimer's disease: APOE genotypes and cognitive function in the Wisconsin Registry for Alzheimer's Prevention. J Geriatr Psychiatry Neurol 2006; 18:1-5.