[GRG] immune booster removes toxic proteins in Alzheimer’s


Contact: David March
NYU Langone Medical Center / New York University School of Medicine

Targeted immune booster removes toxic proteins in mouse model of
Alzheimer’s disease

Clinical trials could begin in 2015

Alzheimer’s disease experts at NYU Langone Medical Center and
elsewhere are reporting success in specifically harnessing a
mouse’s immune system to attack and remove the buildup of toxic
proteins in the brain that are markers of the deadly
neurodegenerative disease.

Reporting on their experiments in the journal Acta Neuropathologica
Communications online Sept. 3, the researchers say the work
advances the development of more effective clinical treatments for
Alzheimer’s because their immune booster reduced both amyloid beta
plaques and tau tangles. Previous immunomodulatory efforts, they
say, were singularly successful in decreasing amyloid beta deposits
but made limited progress in reducing the buildup of tau proteins
that are also a key disease characteristic linked to progressive
brain damage.

“Our study results confirm that precisely boosting the immune
system in mice can work effectively against Alzheimer’s disease, a
treatment model that could very well be applied in humans,” says
senior study investigator and neurologist Thomas Wisniewski, MD, a
professor at NYU Langone.

If further animal testing proves successful, human clinical trials
could begin within a year, says Wisniewski, who also serves as
director of NYU Langone’s Center for Cognitive Neurology and co-
director of its Alzheimer’s Disease Center.

In their written report, the research team calls their findings the
first positive results for targeted stimulation of the natural, or
innate immune system to both prevent the onset of Alzheimer’s
disease in animals bred to develop dementia, and to reverse its
symptoms after the disease has already set in.

Using the dementia-prone mice, the team gave monthly injections of
an immune system booster known as a type B, CpG,
oligodeoxynucleotide that specifically binds to Toll-like receptor
9, or TLR9 for short. Activation of TLR9 triggers an immune
response. Tests in mice that received the immune system booster
injections showed that amyloid plaque formation was 50 percent to
70 percent less than in mice that received no therapy. Reductions
in amyloid beta were almost the same for mice treated early on, at
age 7 months, and before disease onset, compared to mice treated at
age 11 months, which already had mild dementia. Immunostaining
tests on brain tissue in treated mice showed one to two times fewer
damaged neurons containing disease-related tau aggregates than in
untreated mice.

Further cognitive, behavioral testing showed that treated mice made
roughly half the number of mistakes in finding their way in water-
reward mazes than untreated mice. Dementia-associated brain
inflammation was also halved in treated mice, the researchers
report, with “classic signs of a traditional immune response
against both amyloid beta and tau proteins,” as demonstrated by the
presence of immune system cytokines and T-helper cells.

According to researchers, treated mice behaved “almost like normal”
mice that never develop Alzheimer’s-like symptoms.

Wisniewski says that unlike vaccines, which try to trigger an
antibody-mediated stimulation of the body’s immune system, his
team’s new approach attempts to “jump start and rejuvenate” the
brain’s natural microglial cell repair function. The breakdown of
microglial repair — possibly from aging — has been linked for
decades to the formation and removal of amyloid plaques and tau
tangles in Alzheimer’s disease.

Researchers say they selected TLR9 as the immune booster because it
was a known stimulant for removing germs. A bacterial cytosine-
guanosine sequence, or CpG, such as type B, CpG,
oligodeoxynucleotide, was chosen to help activate TLR9 on brain
cells because previous testing had shown it to be effective at
triggering an immune response in both mice and humans, with very
few side effects.

According to study lead investigator Henrieta Scholtzova, MD, PhD,
a clinical fellow at NYU Langone, the latest series of experiments
build on the team’s original observations in 2009, also in mice,
that CpG immune boosting was possible, and could reduce amyloid
plaque formation.

“Now that we have shown that we can influence microglial function
in Alzheimer’s disease, to both prevent and repair tau-damaged
brain tissue, then it is highly plausible that our treatment
approach could also be applied to other neurodegenerative diseases
tied to aging,” says Scholtzova.

Alzheimer’s disease remains the leading cause of dementia
worldwide. The disease, which has no effective treatment, afflicts
some 5.2 million Americans, mostly women, killing up to a half-
million each year.


Funding support for the study was provided by the U.S. National
Institutes of Health. Corresponding federal grant numbers are RO1
AG20245, RO1 NS073502, ULI TR000038, and R01 CA016087. Additional
research support was received from the Seix Dow Foundation and the
Alzheimer’s Association, and grant IIRG-12-239474.

Besides Wisniewski and Scholtzova, other researchers involved in
these experiments were Peter Chianchiano, BA; Jason Pan, BA; Yanjie
Sun; and Fernando Goni, PhD. Additional research support was
provided by Pankaj Mehta, MD, PhD, at the New York State Institute
for Basic Research in Developmental Disabilities on Staten Island,

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About Johnny Adams

My full-time commitment is to slow and ultimately reverse age related functional decline to increase healthy years of life. I’ve been active in this area since the 1970s, steadily building skills and accomplishments. I have a good basic understanding of the science of aging, and have many skills that complement those of scientists so they can focus on science to advance our shared mission. Broad experience Top skills: administration, management, information technology (data and programming), communications, writing, marketing, market research and analysis, public speaking, forging ethical win-win outcomes among stakeholders (i.e. high level "selling"). Knowledge in grant writing, fundraising, finance. Like most skilled professionals, I’m best described as a guy who defines an end point, then figures out how to get there. I enjoy the conception, design, execution and successful completion of a grand plan. Executive Director Gerontology Research Group (GRG). Manages Email discussion forum, web site, meetings and oversees supercentenarian (oldest humans, 110+ years) research. CEO / Executive Director Carl I. Bourhenne Medical Research Foundation (Aging Intervention Foundation), an IRS approved 501(c)(3) nonprofit. http://www.AgingIntervention.org Early contributor to Supercentenarian Research Foundation. Co-Founder Geroscience Healthspan Forum. Active contributor to numerous initiatives to increase healthy years of life. Co-authored book on conventional, practical methods available today to slow the processes of aging – nutrition, exercise, behavior modification and motivation, stress reduction, proper supplementation, damage caused by improper programs, risk reduction and others. Fundamental understanding of, and experience in the genomics of longevity (internship analyzing and curating longevity gene papers). Biological and technical includes information technology, software development and computer programming, bioinformatics and protein informatics, online education, training programs, regulatory, clinical trials software, medical devices (CAT scanners and related), hospital electrical equipment testing program. Interpersonal skills – good communication, honest, well liked, works well in teams or alone. Real world experience collaborating in interdisciplinary teams in fast paced organizations. Uses technology to advance our shared mission. Education: MBA 1985 University of Southern California -- Deans List, Albert Quon Community Service Award (for volunteering with the American Longevity Association and helping an elderly lady every other week), George S. May Scholarship, CA State Fellowship. BA psychology, psychobiology emphasis 1983 California State University Fullerton Physiological courses as well as core courses (developmental, abnormal etc). UCLA Psychobiology 1978, one brief but fast moving and fulfilling quarter. Main interest was the electrochemical basis of consciousness. Also seminars at the NeuroPsychiatric Institute. Other: Ongoing conferences, meetings and continuing education. Aging, computer software and information technology. Some molecular biology, biotech, bio and protein informatics, computer aided drug design, clinical medical devices, electronics, HIPAA, fundraising through the Assoc. of Fundraising Professionals. Previous careers include: Marketing Increasing skill set and successes in virtually all phases, with valuable experience in locating people and companies with the greatest need and interest in a product or service, and sitting across the table with decision makers and working out agreements favorable to all. Information Technology: Management, data analysis and programming in commercial and clinical trials systems, and bioinformatics and protein informatics. As IT Director at Newport Beach, CA based technology organization Success Family of Continuing Education Companies, provided online software solutions for insurance and financial professionals in small to Fortune 500 size companies. We were successful with lean team organization (the slower moving competition was unable to create similar software systems). Medical devices: At Omnimedical in Paramount CA developed and managed quality assurance dept. and training depts. for engineers, physicians and technicians. Designed hospital equipment testing program for hospital services division. In my early 20’s I was a musician, and studied psychology and music. Interned with the intention of becoming a music therapist. These experiences helped develop valuable skills used today to advance our shared mission of creating aging solutions.
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