Newsletter, November 2017

Volume 1, Issue 2

�þ��ҹ��ӰԺ��ѹۿ� State Researchers Help Find Pathologic Hallmarks of Alzheimer’s Disease in Aged Chimpanzee Brains

Researchers have found the first signs of Alzheimer's in chimpanzees

Dementia affects one-third of all people older than 65 years in the United States. The most common cause of dementia is Alzheimer’s disease, a progressive, irreversible brain disease that results in impaired cognitive functioning and other behavioral changes. Humans are considered uniquely susceptible to Alzheimer’s disease, potentially due to genetic differences, changes in brain structure and function during evolution, and an increased lifespan.

WORLD FIRST: NEW POLYMER GOES FOR A WALK WHEN ILLUMINATED

Scientists at Eindhoven University of Technology in the Netherlands and �þ��ҹ��ӰԺ��ѹۿ� have developed a new material that can undulate and therefore propel itself forward under the influence of light. To achieve this, the scientists clamp a strip of this polymer material in a rectangular frame. When illuminated, it goes for a walk all on its own. This small device, the size of a paperclip, is the world’s first machine to convert light directly into walking, simply using one fixed light source. The researchers, including Professor Robin Selinger of �þ��ҹ��ӰԺ��ѹۿ� State’s Liquid Crystal Institute® in the College of Arts and Sciences, published their findings on June 29 in the scientific journal Nature.

�þ��ҹ��ӰԺ��ѹۿ� State Researcher Examines Vaccine Rejection and Hesitancy, Discusses Ways to More Actively Promote Vaccination

Myths about vaccines are causing a decline in confidence, but not necessarily in rates of vaccination

The center of a public health debate is whether parents should have their children vaccinated. Tara Smith, Ph.D., professor of epidemiology at �þ��ҹ��ӰԺ��ѹۿ�’s College of Public Health, challenges statements made by influential individuals who oppose the widespread use of vaccines, and she calls upon her colleagues in the scientific community to speak out to promote vaccination.

�þ��ҹ��ӰԺ��ѹۿ� researchers analyzed the brains of aged chimpanzees to show pathology similar to the human Alzheimer’s disease brain. This image shows tau-positive neuron (black) in proximity to amyloid deposits within blood vessels (red) in an aged chimpanzee brain. However, a published Aug. 1 in provides the most extensive evidence of Alzheimer’s disease brain pathology in a primate species to date. Researchers from �þ��ҹ��ӰԺ��ѹۿ�’s College of Arts and Sciences, along with colleagues from the George Washington University, Yerkes National Primate Research Center, Georgia State University, Barrow Neurological Institute and the Icahn School of Medicine at Mount Sinai, found that the brains of aged chimpanzees, our closest living relatives, show pathology similar to the human Alzheimer’s disease brain.

This research adds to a growing number of studies using an evolutionary perspective to identify differences between humans and chimpanzees that could lead to potential targets for therapeutic interventions in humans.

“Very few studies have investigated Alzheimer’s disease pathology in chimpanzees, the species closest in phylogeny and most genetically related to humans,” said senior author Mary Ann Raghanti, Ph.D., associate professor and interim chair of anthropology at �þ��ҹ��ӰԺ��ѹۿ� State. “Brain samples from great apes, particularly aged individuals, are incredibly scarce, so a study of this size is rare.”

Dysfunction of two proteins, amyloid beta and tau, plays a role in the development of Alzheimer’s disease. In healthy brains, amyloid beta is degraded and eliminated, but in Alzheimer’s disease, overproduction and disrupted clearance of the protein results in the formation of plaques between brain cells called neurons. Amyloid beta in the form of insoluble plaques and soluble peptides initiates changes in tau, another protein found mostly in neurons, that destabilizes the cell’s skeleton. In Alzheimer’s disease, alterations in tau lead to the formation of neurofibrillary tangles and cell death. These neuronal changes result in the onset of dementia.

Analysis of the brain samples for this study began in 2013 in Raghanti’s lab at �þ��ҹ��ӰԺ��ѹۿ� State. The brains were provided by the , which collects the brains of chimpanzees that have died from natural causes at zoos and research centers. The collection started in the mid-1990s for what was then called the Great Ape Aging Project. The National Chimpanzee Brain Resource is supported by the National Institutes of Health (NIH) and is operated in partnership by the George Washington University, Georgia State and Yerkes National Primate Research Center.

By examining brain regions most affected by Alzheimer’s disease pathology in humans, the group demonstrated that amyloid beta plaques and blood vessels were present in all 20 aged chimpanzee brains. Similar to humans, increasingly larger volumes of amyloid beta plaques and blood vessels were found with greater age.

“Interestingly, though, amyloid beta deposition was higher in blood vessels than in plaques, and this correlated with increases in tau lesions,” said Melissa Edler, Ph.D., lead author and former doctoral student in biomedical sciences at �þ��ҹ��ӰԺ��ѹۿ� State. “This suggests that amyloid buildup in the brain’s blood vessels precedes plaque formation in chimpanzees.”

These findings differ from what we see in humans. While approximately 80 percent of Alzheimer’s disease patients also have cerebral amyloid angiopathy, or amyloid beta deposits in the brain’s blood vessels that increase the risk for stroke and dementia, the predominant amyloid beta pathology is plaques. Tau lesions also were found in the forms of neurofibrillary tangles and clusters of tau-positive neurites (i.e., pieces of dying neurons).

“Neurofibrillary tangles are observed in Alzheimer’s disease patients, but the tau-immunoreactive neuritic clusters in the neocortex appear specific to chimpanzees,” said Patrick R. Hof, M.D., Regenstreif professor and vice-chair of neuroscience at Icahn School of Medicine at Mount Sinai. In addition, neurofibrillary tangles pathology was observed in apes that exhibited plaques and moderate or severe cerebral amyloid angiopathy and in one individual with virtually no amyloid beta pathology. “The presence of amyloid and tau pathology in aged chimpanzees indicates these Alzheimer’s disease lesions are not specific to the human brain as generally believed,” Hof continued.

“Whether these pathologies play a key role in age-related cognitive decline requires continued investigation of this species,” said Elliott Mufson, Ph.D., professor and Greening Chair in Aging at the Barrow Neurological Institute.

“We initiated the Great Ape Aging Project 20 years ago because we saw an aging chimpanzee population under human care that would need geriatric attention for disorders similar to those affecting aging humans,” said Joseph Erwin, Ph.D., research professor of anthropology at the George Washington University.

“Findings like those reported in this paper provide significant evidence of the value and need for continued behavioral, cognitive and neurogenomic work with this important species,” said William D. Hopkins, Ph.D., professor of neuroscience at Georgia State and associate research scientist at Yerkes National Primate Research Center, Emory University.

“This study confirms the value of a ‘’ approach to gerontology and the neurobiology of aging for the benefit of humans and apes,” Erwin added.

The article is titled “Aged Chimpanzees Exhibit Pathologic Hallmarks of Alzheimer’s Disease” by Melissa K. Edler, Ph.D.; Chet C. Sherwood, Ph.D.; Richard S. Meindl, Ph.D.; William D. Hopkins, Ph.D.; John J. Ely, Ph.D.; Joseph M. Erwin; Elliott J. Mufson, Ph.D.; Patrick R. Hof, M.D.; and Mary Ann Raghanti, Ph.D (). It appears in Neurobiology of Aging, published by .

This research was supported by grants from the National Science Foundation (BCS-1316829 to M.A.R.), NIH (NS042867, NS073134, and NS092988 to W.D.H. and C.C.S.; AG017802 to J.J.E.; AG014308 to J.M.E.; AG005138 to P.R.H.; AG014449 and AG043775 to E.J.M.), James S. McDonnell Foundation (220020293 to C.C.S.), Sigma Xi, the �þ��ҹ��ӰԺ��ѹۿ� Research Council and �þ��ҹ��ӰԺ��ѹۿ� State’s Graduate Student Senate.

Neurobiology of Aging publishes the results of studies in behavior, biochemistry, cell biology, endocrinology, molecular biology, morphology, neurology, neuropathology, pharmacology, physiology and protein chemistry in which the primary emphasis involves mechanisms of nervous system changes with age or diseases associated with age.

For more information about �þ��ҹ��ӰԺ��ѹۿ� State’s Department of Anthropology, visit www.kent.edu/anthropology.

For more information about research at �þ��ҹ��ӰԺ��ѹۿ� State, visit www.kent.edu/research.

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Photo Caption:
�þ��ҹ��ӰԺ��ѹۿ� researchers analyzed the brains of aged chimpanzees to show pathology similar to the human Alzheimer’s disease brain. This image shows tau-positive neuron (black) in proximity to amyloid deposits within blood vessels (red) in an aged chimpanzee brain.

Media Contacts:
Mary Ann Raghanti, mraghant@kent.edu, 330-672-9354
Emily Vincent, evincen2@kent.edu, 330-672-8595

Return to NOVEMBER 2017 Newsletter
WORLD FIRST: NEW POLYMER GOES FOR A WALK WHEN ILLUMINATED
KENT STATE GEOGRAPHERS RECEIVE TWO RESEARCH GRANTS TO STUDY CLIMATE CHANGE AND WEATHER PATTERNS
KENT STATE RESEARCHER EXAMINES VACCINE REJECTION AND HESITANCY

The maximum speed of the device is equivalent to that of a caterpillar, about half a centimeter per second. The researchers think it can be used to transport small items in hard-to-reach places or to keep the surface of solar cells clean. The researchers placed grains of sand on the strip, and these were removed by the undulating movement. The mechanism is so powerful that the strip can even transport an object that is much bigger and heavier than the device itself uphill.

The motion of the new material is due to the fact that one side contracts in reaction to light while the other side expands, causing it to bulge when illuminated. That deformation disappears instantaneously once the light is gone. Although the material looks transparent to the human eye, it fully absorbs the violet light the researchers used, thus creating a shadow behind it.Scientists at Eindhoven University of Technology in the Netherlands and �þ��ҹ��ӰԺ��ѹۿ� in Ohio have developed a new material that can undulate and therefore propel itself forward under the influence of light. (Photo credit: Bart van Overbeeke)

The scientific team, led by Professor Dick Broer of Eindhoven University of Technology, was able to create a continual undulating movement, using this “self-shadowing” effect. The team members attached a strip of the material in a frame shorter than the strip itself, causing it to bulge. Then the researchers shone a concentrated LED light on it from in front. The part of the strip that is in the light starts to bulge downward, creating a “dent” in the strip. As a consequence, the next part of the strip comes in the light and starts to deform. This way, the “dent” moves backward, creating a continual undulating movement. This sets the device in motion, walking away from the light. When the device is placed upside down, the wave travels in the opposite direction, causing it to walk toward the light.

The research team managed to reach this specific behavior of the material using liquid crystals, familiar in liquid crystal displays or LCDs. The principle relies on the incorporation of a fast-responding, light-sensitive variant in a liquid crystalline polymer network. The researchers engineered a material in such a way that this response is translated to an instantaneous deformation of the strip when illuminated and relaxation when the light is gone. Computer simulations demonstrated the self-shadowing mechanism and explained the directionality of light-driven motion.

The research team’s paper in Nature is titled “Making Waves in a Photoactive Polymer Film.” Joining Selinger and Broer as authors are Anne Hélène Gélébart, Dirk Jan Mulder, Ghislaine Vantomme and Bert Meijer of Eindhoven University of Technology and Michael Varga and Andrew Konya of �þ��ҹ��ӰԺ��ѹۿ� State. The empirical study took place at Eindhoven University of Technology with the corresponding theoretical model being developed at �þ��ҹ��ӰԺ��ѹۿ� State. The research was made possible by subsidies from the Dutch research funding agency NOW, the European Research Council and grants from the U.S. National Science Foundation.

For more information about Eindhoven University of Technology, visit .

For more information about �þ��ҹ��ӰԺ��ѹۿ� State’s Liquid Crystal Institute, visit .

Return to NOVEMBER 2017 Newsletter
KENT STATE RESEARCHERS HELP FIND PATHOLOGIC HALLMARKS OF ALZHEIMER’S DISEASE IN AGED CHIMPANZEE BRAINS
KENT STATE GEOGRAPHERS RECEIVE TWO RESEARCH GRANTS TO STUDY CLIMATE CHANGE AND WEATHER PATTERNS
KENT STATE RESEARCHER EXAMINES VACCINE REJECTION AND HESITANCY

Photo of Tara Smith The article, “,” is published by Oxford Press’ Open Forum Infectious Diseases. In the July 18 article, Smith presents clear and scientifically based arguments to explain why anti-vaccination statements are inaccurate, misleading and even disingenuous. As a recognized expert in microbiology of infectious disease, her concern is that the public can become confused about the safety of vaccines and may be hesitant to immunize themselves and their children.

Widespread refusal of vaccines could lead to many more people becoming infected with vaccine-preventable diseases, such as measles, mumps and influenza.

“Though there is scant evidence that refusal is genuinely increasing in the population, multiple studies have demonstrated concerning patterns of decline of confidence in vaccines, the medical professionals who administer vaccines and the scientists who study and develop vaccines,” Smith wrote.

Her article presents reliable information about vaccine safety while debunking myths that are being circulated and creating misunderstandings among the general public. The article also presents ways that healthcare and infectious disease professionals can actively promote vaccination to friends, family and the people they serve. This information is presented in a way that is sensitive to scientifically trained professionals’ reluctance to advocate on issues in black-and-white terms while also recognizing what is at stake if they do not take action.

For more information about Smith’s research, visit www.kent.edu/publichealth/profile/tara-c-smith-phd.

For more information about �þ��ҹ��ӰԺ��ѹۿ� State’s College of Public Health, visit www.kent.edu/publichealth.

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Photo Caption:
Tara Smith, Ph.D., professor of epidemiology at �þ��ҹ��ӰԺ��ѹۿ�’s College of Public Health, challenges statements made by influential individuals who oppose the widespread use of vaccines, and she calls upon her colleagues in the scientific community to speak out to promote vaccination.

Media Contacts:
Tara Smith, tsmit176@kent.edu, 330-672-3946
Emily Vincent, evincen2@kent.edu, 330-672-8595

Return to NOVEMBER 2017 Newsletter
KENT STATE RESEARCHERS HELP FIND PATHOLOGIC HALLMARKS OF ALZHEIMER’S DISEASE IN AGED CHIMPANZEE BRAINS
KENT STATE GEOGRAPHERS RECEIVE TWO RESEARCH GRANTS TO STUDY CLIMATE CHANGE AND WEATHER PATTERNS
WORLD FIRST: NEW POLYMER GOES FOR A WALK WHEN ILLUMINATED

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