
Gary Arendash
Gary Arendash
Research Professor
Contact
Office: BSF 206
Phone: 813/974-1584
Email:
Education
Ph.D., University of California,
San Francisco Medical Center, 1978.
Research
Neuroscience
My laboratory is interested in understanding the pathogenesis of Alzheimer's Disease, as well developing effective protective strategies and treatments against the disease. My colleagues and I currently have 10 transgenic mouse lines that develop Alzheimer's pathology (amyloid plaques or neurofibrillary tangles), with most of these mouse lines also exhibiting age-related cognitive impairment. My laboratory has emphasized cognitive assessment of Alzheimer's transgenic mice and correlating cognitive performance to neuropathologic and neurochemical measures taken from the same animals. To that end, we have developed an extensive behavioral battery of cognitive, anxiety, and sensorimotor tasks that collectively characterize the behavioral abilities of a given mouse. Recently, my laboratory has utilized high level multi-metric analyses (function analysis, discriminant function analysis, neural networks) that look at behavioral performance across many behavioral measures to determine cognitive impairment and/or treatment effects. Our use of multiple behavioral measures and advanced statistical analysis in Alzheimer's transgenic mice have resulted in a very sensitive behavioral methodology for evaluating protective measures and therapeutics against the disease.
Utilizing our Alzheimer's mice, we have evaluated a variety of possible protections against the disease. In 2000, my colleagues and I published the initial report indicating that vaccinations (with the human protein beta-amyloid) can protect Alzheimer's mice against development of cognitive impairment. Most recently, we have developed a novel vaccine approach against Alzheimer's Disease that is long-lasting and without any deleterious side effects. An additional protection-based approach we have studied is environmental enrichment. Given the epidemiologic evidence that a life-long pattern of high cognitive activity may protect against Alzheimer's Disease, our studies have determined that Alzheimer's mice raised in an enriched environment are indeed protected against cognitive impairment later in life.
In addition to "protection-based" studies, we are also investigating a variety of treatments against Alzheimer's Disease in our transgenic mice that already have cognitive impairment. Both vaccinations and cognitive stimulation result in improved cognitive performance that often attains normal levels. Several dietary strategies are currently being investigated to protect against or treat Alzheimer's Disease in our transgenic mice.
Since last year, I have been closely associated with the Byrd Alzheimer's Center and Research Institute, which is on the USF campus. The Byrd Institute is a state-wide research center, which is bringing Alzheimer's researchers from throughout the state of Florida together in attacking the disease. USF and the Byrd Institute were just awarded an Alzheimer's Disease Research Center (ADRC) grant from NIH, which is the first and only ADRC in the state. Through USF and the ADRC, I will continue my investigations of environmental factors that may protect against or treat Alzheimer's disease.
Recent Publications
Morgan, D., Diamond, D.M., Gottschall, P.E., Ugen, K.E., Dickey, C., Hardy, J.,
Duff, K., Jantzen, P., DiCarlo, G., Wilcock, D., Connor, K., Hatcher, J., Hope,
C., Gordon, M. and G.W. Arendash. A b peptide vaccination prevents memory loss in
an animal model of Alzheimer's disease. Nature 408 : 982-985, 2000.
Arendash, G.W., King, D.L., Gordon, M.N., Morgan, D., Hatcher, J.M., Hope, C.E.
and D.M. Diamond. Progressive, age-related behavioral impairments in transgenic
mice carrying both mutant amyloid precursor protein and presenilin-1 transgenes.
Brain Research 891 : 42-53, 2001.
Gordon, M.N., King, D.L., Diamond, D.M., Jantzen, P.T., Boyett, K.L., Hope, C.E.,
Hatcher, J.M., DiCarlo, G., Gottschall, P.E., Morgan, D. and G.W. Arendash. Correlation
between cognitive deficits and A b deposits in transgenic APP+PS1 mice. Neurobiology
of Aging 22 : 377-386, 2001.
Bjugstad, K.B., Flitter, W.D., Garland , W.A., Philpot, R.M., Kirstein C.L., and
G.W. Arendash. CPI-1189 prevents apoptosis and reduces GFAP immunostaining in a
TNF- a infusion model for AIDS Dementia Complex. J. NeuroVirology 6 : 478-491, 2001.
Arendash, G.W., Gordon, M.N., Diamond, D.M., Hatcher, J.M., Austin , L.A. , Jantzen,
P., DiCarlo, G., Wilcock, D., and D. Morgan. Behavioral assessment of Alzheimer's
transgenic mice following long-term A b vaccination: Task specificity and correlations
between A b deposition and spatial memory. DNA and Cell Biology 11 : 737-744, 2001.
King, D.L. and G.W. Arendash. Maintained synaptophysin immunoreactivity in Tg2576
Transgenic mice during aging: Correlations with cognitive impairment. Brain Research
926 : 58-68, 2002.
King, D.L. and G.W. Arendash. Behavioral characterization of the Tg2576 transgenic
model of Alzheimer's disease through 19 months. Physiology and Behavior 75: 627-642,
2002.
Arendash, G.W. and D.L. King. Intra- and inter-task relationships in a behavioral
test battery given to Tg2576 transgenic mice and controls. Physiology and Behavior
75: 643-652, 2002.
Newman, M.B., Arendash, G.W., Shytle, R.D. and P.R. Sanberg. Nicotine's oxidative
and antioxidant properties in CNS, Life Sciences 71: 2807-2820, 2002.
Austin , L.A. , Arendash, G.W., Gordon, M.N., Diamond, D.M., DiCarlo, G., Dickey,
C., Ugen, K., and D. Morgan. Short-term A b vaccinations do not improve cognitive
performance in cognitively-impaired APP+PS1 mice. Behavioral Neuroscience 117: 478-484,
2003.
Joseph J.A., Denisova, N.A., Arendash, G., Gordon, M., Diamond, D., Shukitt-Hale,
B., and D. Morgan. Blueberry supplementation enhances signaling and prevents behavioral
deficits in Alzheimer' disease model. Nutritional Neuroscience 6: 153-162, 2003
Garcia, M.F., Gordon, M.N., Hutton, M., Lewis, J., McGowan, E., Dickson, D., Morgan,
D., and G.W. Arendash. The retinal degeneration (rd) gene seriously impairs spatial
cognitive performance in normal and Alzheimer's transgenic mice. NeuroReport 15:
73-77, 2004.
Nilsson, L., Arendash, G.W., Low, M.A., Costa, D., Roijani, A., Bales, K.R., Paul,
S.M. and H. Potter. Cognitive impairment in PDAPP mice depends on ApoE and ACT-catalyzed
amyloid formation. Neurobiology of Aging 25: 1153-1167, 2004.
Leighty, R.E., Nilsson, L.N.G., Potter, H., Costa, D.A., Low, M.A., Bales, K.R.,
Paul, S.M., and G.W. Arendash. Use of multimetric statistical analysis to characterize
and discriminate between the performance of four Alzheimer's transgenic mouse lines
differing in A b deposition. Behavioral Brain Research 153: 107-121, 2004.
Arendash, G.W., J. Lewis, R. Leighty, E. McGowan, J. Cracchiolo, M. Hutton, and
M.F. Garcia. Multi-metric behavioral comparison of APPsw and P301L models for Alzheimer's
Disease: Linkage of poorer cognitive performance to tau pathology in Forebrain.
Brain Research 1012: 29-41, 2004
Arendash, G.W., Garcia, M.F., Costa, D.A., Cracchiolo, J.R., Wefes, I.M., and H.
Potter. Environmental enrichment improves cognition in Alzheimer's transgenic mice
despite stable b -amyloid deposition, Neuroreport 15: 1751-1754, 2004.
Jensen, M., Mottin, M.D., Cracchiolo, J.R., Leighty, R.E., and G.W. Arendash. Life-long
immunization with human b -amyloid (1-42) protects AD transgenic mice against cognitive
impairment throughout aging. Neuroscience 130: 667-684, 2005.
Bjugstad K.B. and G.W. Arendash. Intracerebroventricular infusions of Gp120 inhibit
weight gain and induce atrophy in the hippocampus and neostriatum without affecting
cognition.
J. NeuroAIDS 2: 15-32, 2005.