NIH-Supported Study Looks for Earliest Changes in the Brain That May Lead to Alzheimer’s Disease

By Joel Ross | June 2, 2010

My readers often think and ask, “When is the best time to get tested for possible Alzheimer’s Disease”.
The answer is simple: AS SOON AS POSSIBLE! This study will help identify the biomarkers (this can be an MRI of the brain, analysis of body fluids such as blood, spinal flood, brain imaging using amyloid markers, et al). Please consider volunteering to help yourself and the future generations of individuals who will be diagnosed with dementia of the Alzheimer’s type or what I call, “Amyloid Associated Memory Impairment (AAMI for short).”

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
National Institute on Aging (NIA)
For Immediate Release: June 2, 2010

CONTACT:
Peggy Vaughn, 301-496-1752,

NIH-Supported Study Looks for Earliest Changes in the Brain That May Lead to
Alzheimer’s Disease

Volunteers are being sought for a clinical study examining the subtle
changes that may take place in the brains of older people many years before
overt symptoms of Alzheimer’s disease appear. Researchers are looking for
people with the very earliest complaints of memory problems that affect
their daily activities. The study will follow participants over time, using
imaging techniques developed to advance research into changes taking place
in the structure and function of the living brain, as well as biomarker
measures found in blood and cerebrospinal fluid.

The National Institute on Aging (NIA), part of the National Institutes of
Health, and the NIH Office of the Director are funding the $24 million,
two-year Alzheimer’s Disease Neuroimaging Initiative Grand Opportunity
(ADNI-GO) study. Researchers seek to recruit 200 volunteers between the
ages of 55 and 90 who may be transitioning from normal cognitive aging to an
early stage of amnestic mild cognitive impairment (aMCI), a condition that
may progress to Alzheimer’s disease. Participants may volunteer at 51 sites
across the United States.

“ADNI-GO is part of an ongoing effort to establish imaging and fluid
biomarker measures of Alzheimer’s disease from the onset of mild symptoms to
the advanced stages of the disease process,” said NIA Director Richard J.
Hodes, M.D. “By advancing understanding of the full spectrum of the disease,
we’ll be better able to identify who is at risk, track progression of the
disorder, and devise measurements to test the effectiveness of potential
prevention or treatment strategies.”

The grant expands the efforts of the Alzheimer’s Disease Neuroimaging
Initiative (ADNI), a research partnership supported primarily by the NIA
with private-sector support through the Foundation for the National
Institutes of Health ADNI began in 2004 to establish neuroimaging and
biomarker measures to track the changes taking place in the brains of 800
older people either free of symptoms or diagnosed with late-stage MCI and
early Alzheimer’s disease. ADNI is led by the Northern California Institute
for Research and Education, a nonprofit foundation affiliated with the San
Francisco VA Medical Center. Michael Weiner, M.D., is the principal
investigator.

The new ADNI-GO effort enables researchers to continue studying nearly 500
of the original ADNI volunteers, while expanding the study to include the
new participants with early amnestic MCI. Newly enrolled participants and
some original study volunteers will undergo a lumbar puncture to collect
cerebrospinal fluids.

“The objective of ADNI-GO is to add to the power of the original study by
increasing our knowledge of the sequence and timing of events involved in
the disease from its earliest measureable point, perhaps even
pre-symptomatically, to overt Alzheimer’s disease,” said Marcelle
Morrison-Bogorad, Ph.D., director of NIA’s Division of Neuroscience.

The ability to gain this knowledge is only possible, Morrison-Bogorad
emphasized, through the generosity of research volunteers. “The research
community is deeply grateful to the volunteers, and their families and
friends, who give of themselves in this search for a cure for or prevention
of Alzheimer’s disease,” she said.

To volunteer or learn more about the study, contact the NIA Alzheimer’s
Disease Education and Referral Center by calling 1-800-438-4380 or by going
to . Volunteers must speak English or Spanish
and have a person willing to assist them during at least five clinic visits
and with telephone contacts from researchers.

Data from the study will be posted to a publicly accessible database
available to qualified researchers worldwide. To date, more than 800
researchers have signed up for ADNI database access. Investigators may apply
for access through the database Web site at www.loni.ucla.edu/ADNI. In
addition, qualified scientists may also ask for access to the cerebrospinal
fluid and blood samples.

In addition to NIA, the original ADNI study involved other federal partners:
the National Institute of Biomedical Imaging and Bioengineering, also part
of NIH, and the U.S. Food and Drug Administration, another agency of the
U.S. Department of Health and Human Services. To learn more about ADNI
advances and the private-public partnership supporting the research, go to
.

The NIA leads the federal government effort conducting and supporting
research on the biomedical, social and behavioral issues of older people.
For more information on aging-related research and the NIA, go to
. The NIA provides information on age-related cognitive
change and neurodegenerative disease specifically at its Alzheimer’s Disease
Education and Referral (ADEAR) Center site at .
To sign up for e-mail alerts about new findings or publications, please
visit either website.

FNIH was established by the United States Congress to support the mission of
the National Institutes of Health-improving health through scientific
discovery. The foundation identifies and develops opportunities for
innovative public-private partnerships involving industry, academia and the
philanthropic community. A non-profit, 501(c)(3) corporation, the foundation
raises private-sector funds for a broad portfolio of unique programs that
complement and enhance NIH priorities and activities. The foundation’s Web
site address is .

The National Institutes of Health (NIH) — The Nation’s Medical Research
Agency — includes 27 Institutes and Centers and is a component of the U.S.
Department of Health and Human Services. It is the primary federal agency
for conducting and supporting basic, clinical and translational medical
research, and it investigates the causes, treatments, and cures for both
common and rare diseases. For more information about NIH and its programs,
visit .

——————————————-
The 51 study sites recruiting volunteers are located in:

Albany, N.Y.
Amherst, N.Y.
Ann Arbor, Mich.
Atlanta
Baltimore
Birmingham, Ala.
Boston
Charleston, S.C.
Chicago
Cleveland
Dallas
Durham, N.C.
Hartford, Conn.
Houston
Indianapolis
Irvine, Calif.
Jacksonville, Fla.
Kansas City, Kan.
Las Vegas
Lebanon, N.H.
Lexington, Ky.
Los Angeles
Madison, Wis.
Miami
New Haven, Conn
New York City
Palo Alto, Calif.
Philadelphia
Phoenix
Pittsburgh
Portland, Ore.
Providence, R.I.
Rochester, Minn.
Rochester, N.Y.
Sacramento, Calif.
San Diego
San Francisco
St. Louis
Sun City, Ariz.
Washington
West Palm Beach, Fla.
Winston-Salem, N.C.

This NIH News Release is available online at:
.

To subscribe (or unsubscribe) from this list, go to
.

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No prevention measures work to reduce risk of Alzheimer’s Disease (so far)

By Joel Ross | April 29, 2010

The very well respected “independent” panel of the National Institutes of Health has now announced preventative measures are not effective in reducing your risk of AD.
However, eating right, exercizing regularly, staying happy are all common sense approaches to overall well being, but they have not been shown to lower one’s risk of progressive memory loss from Alzheimer’s Disease. Please read on below:

Subject: INDEPENDENT PANEL FINDS INSUFFICIENT EVIDENCE TO SUPPORT PREVENTIVE MEASURES FOR ALZHEIMER’S DISEASE

U.S. Department of Health and Human Services
NATIONAL INSTITUTES OF HEALTH NIH News
NIH Office of the Director (OD)
Office of Medical Applications of Research (OMAR)

For Immediate Release: Wednesday, April 28, 2010

CONTACT: Lisa Ahramjian, 301-496-4999,

INDEPENDENT PANEL FINDS INSUFFICIENT EVIDENCE TO SUPPORT PREVENTIVE MEASURES
FOR ALZHEIMER’S DISEASE

Many preventive measures for cognitive decline and for preventing
Alzheimer’s disease — mental stimulation, exercise, and a variety of
dietary supplements — have been studied over the years. However, an
independent panel convened this week by the National Institutes of Health
determined that the value of these strategies for delaying the onset and/or
reducing the severity of decline or disease hasn’t been demonstrated in
rigorous studies.

“Alzheimer’s disease is a feared and heart-breaking disease,” said Dr.
Martha L. Daviglus, conference panel chair and professor of preventive
medicine and medicine at Northwestern University, Chicago. “We wish we could
tell people that taking a pill or doing a puzzle every day would prevent
this terrible disease, but current evidence doesn’t support this.”

The panel’s assessment of the available evidence revealed that progress to
understand how the onset of these conditions might be delayed or prevented
is limited by inconsistent definitions of what constitutes Alzheimer’s
disease and cognitive decline. Other factors include incomplete
understanding of the natural history of the disease and limited
understanding of the aging process in general. The panel recommended that
the research community and clinicians collaborate to develop, test, and
uniformly adopt objective measures of baseline cognitive function and
changes over time.

Although many non-modifiable risk factors have been examined, age is the
strongest known risk factor for Alzheimer’s disease. Additionally, a genetic
variant of a cholesterol-ferrying protein (apolipoprotein E), has strong
evidence of association with the risk for developing Alzheimer’s disease.
Although it is hoped that improved understanding of genetic risk factors may
ultimately lead to effective therapies, currently these associations are
primarily useful in the clinical research setting.

The panel determined that there is currently no evidence of even moderate
scientific quality supporting the association of any modifiable
factor-dietary supplement intake, use of prescription or non-prescription
drugs, diet, exercise, and social engagement-with reduced risk of
Alzheimer’s disease. The evidence surrounding risk reduction for cognitive
decline is similarly limited. Low-grade evidence shows weak associations
between many lifestyle choices and reduced risk of Alzheimer’s disease and
cognitive decline.

Although there is little evidence that these interventions lessen cognitive
decline, some are not necessarily harmful and may confer other benefits.
However, the panel also emphasized the need for enhanced public
understanding that these proposed prevention strategies are currently, at
best, only loosely associated with improved outcomes. This means that
carefully-designed randomized studies may reveal that these modifiable
factors enhance, detract, or have no effect on preventing Alzheimer’s
disease and cognitive decline.

“These associations are examples of the classic chicken or the egg quandary.
Are people able to stay mentally sharp over time because they are physically
active and socially engaged or are they simply more likely to stay
physically active and socially engaged because they are mentally sharp?”
added Dr. Daviglus. “An association only tells us that these things are
related, not that one causes the other.”

The panel found that certain chronic diseases, such as diabetes and
depression, and risk factors such as smoking are associated with increased
risk of both Alzheimer’s disease and cognitive decline. However, studies
have not yet demonstrated that these medical or lifestyle factors actually
cause or prevent Alzheimer’s disease or cognitive decline, only that they
are related.

There is insufficient evidence to support the use of pharmaceuticals or
dietary supplements to prevent Alzheimer’s disease or cognitive decline.
Ongoing studies exploring factors including but not limited to physical
activity, omega-3 fatty acids (typically found in fish), antihypertensive
medications, and cognitive engagement may provide new insight into
Alzheimer’s disease and cognitive decline prevention.

The panel made a variety of recommendations to shape the future research
agenda and fill identified gaps, while acknowledging that advancing our
understanding of these complex conditions in order to develop conclusive,
evidence-based prevention recommendations will require considerable time and
resources. For example, the panel advocated launching long-term,
longitudinal studies to better characterize the natural history and
progression of these diseases in the community. They also recommended the
establishment of registries for Alzheimer’s disease and cognitive decline,
modeled on existing registries for cancer.

Extensive research over the past 20 years has provided important insights on
the nature of Alzheimer’s disease and cognitive decline and the magnitude of
the problem. Nevertheless, there remain important and formidable challenges
in conducting research on these diseases, particularly in the area of
prevention. There are numerous ongoing or planned investigations which may
offer promising new insights regarding the causes and prevention of these
diseases.
An updated version of the panel’s draft consensus statement, which
incorporates comments received during this morning’s public session, will be
posted later today at .

The panel will hold a press telebriefing to discuss their findings today at
2:00 p.m. EDT. To participate, call 1-888-428-7458 (US) or 201-604-1577
(International) and reference the NIH Alzheimer’s conference. Audio playback
will be available shortly after conclusion of the telebriefing, by calling
1-888-632-8973 (U.S.) or 201-499-0429 (International) and entering replay
code 35986458.

The conference was sponsored by the NIH Office of Medical Applications of
Research and the National Institute on Aging, along with other NIH and
Department of Health and Human Services components. This conference was
conducted under the NIH Consensus Development Program, which convenes
conferences to assess the available scientific evidence and develop
objective statements on controversial medical issues.

The 15-member panel included experts in the fields of preventive medicine,
geriatrics, internal medicine, neurology, neurological surgery, psychiatry,
mental health, human nutrition, pharmacology, genetic medicine, nursing,
health economics, health services research, and family caregiving. A
complete listing of the panel members and their institutional affiliations
is included in the draft conference statement. Additional materials,
including panel bios, photos, and other related resources, are available at
. Interviews with panel members
can be arranged by contacting Lisa Ahramjian at 301-496-4999 or AhramjianL@od.nih.gov>.

The conference was webcast live and will be archived shortly. Links to the
archived webcast will be available at
.

Individuals interested in obtaining resources for patients and families
affected by Alzheimer’s disease may wish to contact the National Institute
on Aging’s Alzheimer’s Disease Education and Referral Center at
1-800-438-4380 or .

In addition to the material presented at the conference by speakers and the
comments of conference participants presented during discussion periods, the
panel considered pertinent research from the published literature and the
results of a systematic review of the literature. The systematic review was
prepared through the Agency for Healthcare Research and Quality
Evidence-based Practice Centers (EPC) program, by the Duke University
Evidence-based Practice Center. The EPCs develop evidence reports and
technology assessments based on rigorous, comprehensive syntheses and
analyses of the scientific literature, emphasizing explicit and detailed
documentation of methods, rationale, and assumptions. The evidence report on
preventing Alzheimer’s disease and cognitive decline is available at
.

The panel’s statement is an independent report and is not a policy statement
of the NIH or the federal government. The NIH Consensus Development Program
was established in 1977 as a mechanism to judge controversial topics in
medicine and public health in an unbiased, impartial manner. NIH has
conducted 122 consensus development conferences, and 34 state-of-the-science
(formerly “technology assessment”) conferences, addressing a wide range of
issues. A backgrounder on the NIH Consensus Development Program process is
available at .

The Office of the Director, the central office at NIH, is responsible for
setting policy for NIH, which includes 27 Institutes and Centers. This
involves planning, managing, and coordinating the programs and activities of
all NIH components. The Office of the Director also includes program offices
which are responsible for stimulating specific areas of research throughout
NIH. Additional information is available at .

This NIH News Release is available online at:
.

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Don’t always believe what is published

By Joel Ross | April 16, 2010

If you read this account of GAMMAGARD one would feel it is the “end all” for Alzheimer’s Disease. However please also review my comments on the published results:

Apparently, the study was conducted in the US. The way of presenting the results of this study is very misleading. Baxter presented the study as a 18-month trial but actually this was an open label extension phase of a very small 6-month, placebo-controlled study which results were never fully disclosed. In summary, there was a group of patients (n = 16) that took Gammagard for 18 months. Another group took placebo for 6 months and than Gammagard for other 12 months. The decline on ADAS-Cog of the group that initially took placebo was huge for a 18-month period (15 points!) and was significantly higher than the group that took Gammagard (6 points, p = 0.013). The normal decay in mild-to-moderate AD patients on placebo in a 18-month period is about 6 points. The 15-point decay observed in the 6 patients that initially took placebo-and then Gammagard was simply due by chance in a very small sample size (n = 6) and explains the significant difference compared to the group that took Gammagard continuously. Please note that this is not a double-blind study.

Baxter And New York-Presbyterian/Weill Cornell Announce 18-Month Data From Phase II Study Of GAMMAGARD In Patients With Alzheimer’s Disease
Article Date: 15 Apr 2010 – 1:00 PDT

Baxter International Inc. (NYSE: BAX) and New York-Presbyterian Hospital/Weill Cornell Medical Center today announced results of an 18-month Phase II clinical study of GAMMAGARD LIQUID and GAMMAGARD S/D [Immune Globulin Intravenous (Human)] (marketed as KIOVIG outside of the U.S.) for mild-to-moderate Alzheimer’s disease. This marked the first announcement of clinical trial results measuring function and cognition in patients who received uninterrupted GAMMAGARD for a period of 18 months.

The study measured function using the Alzheimer’s Disease Cooperative Study-Clinical Global Impression of Change rating (ADCS-CGIC) and measured cognition using the Alzheimer’s Disease Assessment Scale-Cognitive Subscale score (ADAS-Cog). After 18 months, patients (n=14) who received GAMMAGARD continuously averaged approximately 1.36 points higher than patients (n=7) who initially received placebo (-0.64 vs. -2.0, p=0.011) on the ADCS-CGIC. Patients (n=14) who received GAMMAGARD continuously declined by approximately 9.15 fewer ADAS-Cog points than patients (n=6) who initially received placebo (approximately 6 point decline vs. 15 point decline, p=0.013).

The data are being presented at the American Academy of Neurology (AAN) annual meeting in Toronto by the principal investigator for the trial, Dr. Norman Relkin, and Dr. Diamanto Tsakanikas. Dr. Relkin is the director of the Memory Disorders Program and a behavioral neurologist and neuroscientist at the New York-Presbyterian Hospital/Weill Cornell Medical Center, and associate professor of clinical neurology at Weill Cornell Medical College. Dr. Tsakanikas is a clinical assistant attending neuropsychologist at New York-Presbyterian Hospital/Weill Cornell Medical Center and instructor of neuropsychology in the Department of Neurology & Neuroscience at Weill Cornell Medical College. The study was supported by Baxter, the Citigroup Foundation, and The Clinical Translational Science Center (CTSC) of Weill Cornell Medical College.

Being presented for the first time, MRI analyses showed that patients who received GAMMAGARD continuously for 18 months experienced decreased mean annual ventricular enlargement rates in their brains (6.7%), compared to control patients who initially received placebo (12.3%, p=0.048). The decreased rates of ventricular enlargement correlated with clinical outcomes in patients who received continuous GAMMAGARD for 18 months, as measured using the ADCS-CGIC (r= 0.523, p= 0.018) and the ADAS-Cog (r=0.64, p=0.0041). In addition, patients who received GAMMAGARD continuously for 18 months experienced lower mean annual whole brain atrophy rates (-1.58%), compared to control patients who initially received placebo (-2.24%, p=NS). The decreased rates of whole brain atrophy correlated with clinical outcomes in patients who received continuous GAMMAGARD for 18 months, as measured using the ADCS-CGIC (r= 0.64, p= 0.0041) and the ADAS-Cog (r=0.42, p=0.076).

“The cognitive and functional outcomes and neuroimaging results from this 18-month Phase II study in participants receiving GAMMAGARD continuously clearly support continued evaluation for Alzheimer’s disease in a larger number of patients,” said Dr. Paul Aisen, director of the Alzheimer’s Disease Cooperative Study. “The important next step is to fully enroll and complete the ongoing Phase III study of GAMMAGARD, in hope of confirming these Phase II findings and fully understanding GAMMAGARD’s potential benefit in Alzheimer’s disease.”

The ongoing Phase III study of GAMMAGARD, called the Gammaglobulin Alzheimer’s Partnership (GAP) Study, is designed to evaluate the potential of GAMMAGARD for mild-to-moderate Alzheimer’s disease. The study includes 35 actively enrolling sites at leading academic centers in the United States that are members of The Alzheimer’s Disease Cooperative Study (ADCS), with an additional 12 sites pending in the U.S. and Canada. Study participants will be evaluated on clinical scales for cognition and function over 18 months. Biomarker and neuroimaging tests will be performed in order to measure GAMMAGARD’s potential effect on disease progression. Alzheimer’s patients and their caregivers can find study details and learn more about participation by visiting http://www.GAPSTUDY.com or calling 1-877-55-GAPSTUDY (1-877-554-2778). The study is sponsored by Baxter and partially funded by the National Institutes of Health (NIH) through the Alzheimer’s Disease Cooperative Study (ADCS).

Baxter plans to initiate a second, concurrent Phase III study of GAMMAGARD for mild-to-moderate Alzheimer’s disease to confirm the Phase II results in more patients. The Phase II results represent the first study in Alzheimer’s disease where all three measures – cognitive, functional and neuroimaging – had positive data and were statistically significant.

Alzheimer Dementia Study
Phase 3 Investigational Trial – Seeking Patients Now
www.ConcertStudy.com

Volunteers Needed
Learn About a Current Alzheimer’s Study-Find Out if You are Eligible
www.studyforalz.com
“Baxter is encouraged by the 18-month Phase II results for GAMMAGARD for Alzheimer’s disease. Based on the strength of these data, we plan to initiate a second Phase III study of GAMMAGARD for Alzheimer’s disease,” said Hartmut Ehrlich, M.D., vice president of research and development for Baxter BioScience. “The new study will collect additional evidence to support GAMMAGARD’s use in mild-to-moderate Alzheimer’s disease and, with our ongoing Phase III study, support filing for registration in this indication. We will work closely with FDA on appropriate next steps and look forward to making continued progress studying GAMMAGARD’s potential benefit in Alzheimer’s disease and other neurology indications.”

Baxter’s commitment to advancing the scientific and clinical knowledge around GAMMAGARD in several neurological applications includes multiple late-stage clinical trials. In addition to the ongoing Phase III trial studying GAMMAGARD LIQUID in Alzheimer’s disease, Baxter is currently enrolling patients into a Phase III trial studying GAMMAGARD LIQUID in multifocal motor neuropathy (MMN). A Phase III trial studying GAMMAGARD LIQUID in chronic inflammatory demyelinating polyneuropathy (CIDP) is planned to begin later this year.

Phase II Study Design

In the double-blind, placebo-controlled Phase II study, 24 patients in the U.S. with mild-to-moderate Alzheimer’s disease were randomly assigned to receive GAMMAGARD (16 patients), or saline placebo (8 patients) for six months. After six months, the group initially receiving placebo subsequently received various doses of GAMMAGARD while the other 16 patients had uninterrupted GAMMAGARD at the initially assigned dose. The study included a comparison of four dosing regimens of GAMMAGARD, with doses ranging from 0.2 g/kg every two weeks to 0.8 g/kg every four weeks.

Cognitive, behavioral and functional measures were collected at baseline and every three months thereafter. The primary endpoints of the Phase II trial were global function, as assessed by the ADCS-CGIC, and cognitive function, as measured by the ADAS-Cog. Safety and tolerability of GAMMAGARD in Alzheimer’s patients were also assessed relative to placebo. Secondary endpoints included effects on neuroimaging and biomarkers related to beta amyloid, a peptide related to Alzheimer’s disease.

Phase III Study Design

The ongoing Phase III trial is a prospective, 18-month, randomized, double-blind, placebo-controlled, two dose-arm, parallel groups in 360 subjects of both genders, ages 50 to 89 years old, with Alzheimer’s dementia of mild-to-moderate severity. The study will evaluate whether intervention with GAMMAGARD LIQUID results in a significantly slower rate of decline of cognitive and other functions compared to placebo. This trial is expected to be the first of two pivotal Phase III trials required to support filing for regulatory approval for GAMMAGARD LIQUID for Alzheimer’s disease.

Efficacy will be assessed by two co-primary endpoints: global clinical outcome as assessed by the Alzheimer’s Disease Cooperative Study-Clinical Global Impression of Change rating (ADCS-CGIC), and cognitive outcomes using the Alzheimer’s Disease Assessment Scale-Cognitive Subscale score (ADAS-Cog).

Secondary endpoints to be assessed include behavioral, functional and quality of life outcome measures. Other study endpoints will include several plasma, cerebrospinal fluid, and neuroimaging biomarkers to assess disease progression and response to GAMMAGARD.

About GAMMAGARD LIQUID

GAMMAGARD LIQUID is indicated for the treatment of primary immunodeficiency disorders associated with defects in humoral immunity. These include, but are not limited to, congenital X-linked agammaglobulinemia, common variable immunodeficiency, Wiskott-Aldrich syndrome, and severe combined immunodeficiencies.

Important Risk Information

GAMMAGARD LIQUID is contraindicated in patients with known anaphylactic or severe hypersensitivity responses to Immune Globulin (Human). Patients with severe selective IgA deficiency (IgA < 0.05 g/L) may develop anti-IgA antibodies that can result in a severe anaphylactic reaction.

Immune Globulin Intravenous (Human) products have been reported to be associated with renal dysfunction, acute renal failure, osmotic nephrosis, and death. Patients predisposed to acute renal failure include patients with any degree of pre-existing renal insufficiency, diabetes mellitus, age greater than 65, volume depletion, sepsis, paraproteinemia, or patients receiving known nephrotoxic drugs. Especially in such patients, IGIV products should be administered at the minimum concentration available and the minimum rate of infusion practicable. While these reports of renal dysfunction and acute renal failure have been associated with the use of many of the licensed IGIV products, those containing sucrose as a stabilizer accounted for a disproportionate share of the total number.

Glycine, an amino acid, is used as a stabilizer. GAMMAGARD LIQUID does not contain sucrose.

GAMMAGARD LIQUID is made from human plasma. It may carry a risk of transmitting infectious agents, viruses, and theoretically, the Creutzfeldt-Jakob disease (CJD) agent.

Components used in the packaging of this product are latex-free.

Thrombotic events have been reported in association with IGIV. Patients at risk may include those with a history of atherosclerosis, multiple cardiovascular risk factors, advanced age, impaired cardiac output, and/or known or suspected hyperviscosity, hypercoagulable disorders, and prolonged periods of immobilization.

IGIV products can contain blood group antibodies that may cause a positive direct antiglobulin reaction and, rarely, hemolysis.

Aseptic meningitis syndrome (AMS) has been reported to occur infrequently in association with IGIV treatment. Discontinuation of IGIV treatment has resulted in remission of AMS within several days without sequelae.

Various mild and moderate reactions, such as headache, fever, fatigue, chills, flushing, dizziness, urticaria, wheezing or chest tightness, nausea, vomiting, rigors, back pain, chest pain, muscle cramps, and changes in blood pressure may occur with infusions of Immune Globulin Intravenous (Human).

Source
New York-Presbyterian Hospital/Weill Cornell Medical Center
Baxter International Inc.

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Breakthrough Imaging test for the eluse Amyloid Plaque?

By Joel Ross | April 16, 2010

I have been an investigator for AVID Radiopharmaceuticals and participated (and currently participate) in a study where there new imaging agent is being used to detect presence of the very sticky and possibly causative agent in memory loss due to Alzheimer’s Disease called “amyloid”. My readers have read my blogs about amyloid (from the Latin meaning “starch like” or sticky). It is strongly believed by many clinical neuroscientists including yours truly, that the absence of amyloid would be strong evidence against any memory loss to to “impending” or “prodromal Alzheimer’s Disease”. Thus if a scan such as that being used by AVID Radiopharmaceuticals is negative for amyloid, the patient can be fairly reassured Alzheimer’s Disease is unlikely present. However, the mere presence of a positive scan for amyloid does not mean you have Alzheimer’s Disease, but perhaps a pre-Alzheimer’s amyloid state of affairs in your brain. Put another way, having amyloid positive scan cannot be a healthy finding, but not necessarily indicative of Alzheimer’s Disease but it might certainly put you at high risk if more amyloid starts to destroy brain cells. Also, post morten studies have been done and replicated in elderly patients who died without any measurable cognitive impairment (no dementia in life) only to find a good deal of amyloid in the brain post mortem. What does this mean? I believe it suggests some older people can “tolerate” a certain load of the toxic amyloid and never have brain cell death sufficiently severe to cause memory issues. Read below of the very small but exciting news just released yesterday in Toronto.

Positive Interim Results From Phase III Trial Of Amyloid Imaging Agent Florbetapir F18 Presented At American Academy Of Neurology Annual Meeting Article Date: 15 Apr 2010 – 18:00 PDT

Avid Radiopharmaceuticals, Inc. (”Avid”) today announced the presentation of interim data from its landmark florbetapir “Image-to-Autopsy” Phase III study. These data come from the first cohort of subjects in the trial and are the first ever Phase III results for an agent designed to image Alzheimer’s disease pathology. Today, Alzheimer’s disease can only be definitely diagnosed by microscopic detection of beta-amyloid at autopsy. The goal of Avid’s Phase III trial is to test the ability of florbetapir to image beta-amyloid in living patients.

The interim data showed that florbetapir PET imaging results in patients correlated with the levels of beta-amyloid pathology later found in their brains at autopsy. Dr. Adam Fleisher, Associate Director of Brain Imaging at Banner Alzheimer’s Institute, presented the analysis at the 2010 Annual Meeting of the American Academy of Neurology in Toronto, ON.

Dr. Fleisher commented “These preliminary results are very encouraging for the field of amyloid imaging and the future management of Alzheimer’s disease. The data suggest that florbetapir imaging may offer an opportunity to detect amyloid plaques in-life. Knowing if a patient has Alzheimer’s pathology might lead to better patient management — for example, if a patient has memory loss but no amyloid pathology, we could rule-out Alzheimer’s disease, and instead focus on looking for other causes for their symptoms.”

Dr. Fleisher reported the results from the analysis of the first six subjects of the florbetapir “Image-to-Autopsy” Phase III study. The data from this cohort demonstrated that the florbetapir PET images correlated strongly with the post mortem histopathology findings. The PET images not only correctly identified which subjects had beta-amyloid deposits, but also showed where in the brain the deposits had accumulated. The full trial data are expected to be available later this year.

Avid’s florbetapir was the first beta-amyloid imaging compound to enter multi-center, IND clinical studies in the U.S., and has now been studied in more than a dozen trials in over 700 subjects ranging from cognitively normal individuals to those with Alzheimer’s dementia. As well as the pivotal Phase III Image-to-Autopsy study, additional clinical studies in the E.U., South America, Australia and Asia are also being conducted.

About Alzheimer’s Disease and Beta-Amyloid Plaque Deposits

Alzheimer’s disease, a chronic neurodegenerative condition that currently affects over 5 million Americans1, cannot be definitively diagnosed until after death, when a brain autopsy is performed on a patient and evidence of beta-amyloid plaque deposits in the brain – which are a hallmark pathology of the disease – can be found. Accurate diagnosis during life can be challenging, particularly in the early stages of disease, when symptoms are mild and non-definitive and can be mistaken for those of other treatable conditions. Florbetapir, used with positron emission tomography (PET) technology is being assessed for the ability to detect beta-amyloid plaque deposits in-vivo, potentially offering clinically useful diagnostic insight at an early stage.

1 Source: Alzheimer’s Association 2010 Alzheimer’s Disease Facts and Figures

Source
Avid Radiopharmaceuticals, Inc.

Topics: Alzheimer’s Disease, Amyloid Associated Memory Impairment, Uncategorized | 1 Comment »

A Virus transferring a new Alzheimer’s Disease mediatication directly into the brain!

By Joel Ross | April 8, 2010

Local Researchers To Test First Transfer Agent To Improve Brain Function In Alzheimer’s Disease Patients

A phase II study (meaning it is the second step in getting the drug to reach approval in a four step process, meaning phase I, II, III and then IV) is being launced which is hoping to deliver a piece of genetic matter into the brains of Alzheimer’s Disease patients.

Is this a long shot or sure shot? Answer is unknown. The current treatments do not in any way slow disease progression, but rather for a period 6-12 months in some, repeat SOME Alzheimer’s Disease sufferers slow symptoms. There are many phase I, II and some even in Phase III (such as those being conducted at my 3 Memory Enhancement Centers) testing novel medications that try to actually slow the disease from progressing downhill.

Please read below for the updated information on this gene transfer using a virus injected directly in the brain!

Researchers at Banner Sun Health Research Institute are about to start the first Phase 2 research study to test a gene transfer agent for Alzheimer’s disease (AD). AD is a degenerative and ultimately fatal disorder affecting as many as five million Americans and that number is expected to soar to more than 11 million by 2040. For the first time in AD research, scientists are about to test the efficacy of a gene transfer therapy called CERE-110.

Previously, CERE-110 was studied in a small study to assess safety. These studies showed that CERE-110 can induce long-term production of Nerve Growth Factor (NGF) by brain cells. Researchers are now seeking 50 study participants with mild to moderate AD for a Phase 2 clinical study at 12 U.S. research sites, including Banner Sun Health research Institute.

The study utilizes a viral-based gene transfer system that makes NGF, a naturally occurring protein that maintains nerve cell survival in the brain. A neurosurgeon injects CERE-110 directly into the nucleus basalis of Meynert (NBM) of the brain, an area where neuron death occurs in AD.

“The reasoning behind this study is that NGF is known to support the survival and function of the neurons that deteriorate in AD,” says Marwan Sabbagh MD, director of clinical research at Banner Sun Health Research Institute. “These neurons produce the chemical acetylcholine, which is important in memory and cognitive function; restoration of this system’s function may improve memory in AD patients.”

Previous Research

A Phase 1 study was conducted at University of California San Diego. The 10 subjects underwent cognitive testing, measures of activities of daily living, and MRI and PET (positron emission tomography) scans. Researchers observed increases in brain metabolism in several cortical regions of the brain at six months and 12 months in some of the participants, as compared to other severity-matched individuals with AD, suggesting a potential reversal of patterns typically observed in AD.

The Phase 2 Clinical Study

In this blinded study, all eligible participants will be randomized by chance to one of two treatment groups: half will receive CERE-110 and half will receive placebo (inactive drug). Once the study is completed, and if the results are promising, participants in the placebo group will be eligible to receive CERE-110.

The NGF study is being conducted by the Alzheimer’s Disease Cooperative Study (ADCS), a nationwide consortium of research centers and clinics supported by the National Institute on Aging (NIA), part of the National Institutes of Health, and coordinated by the University of California San Diego. Ceregene, Inc., the study sponsor, is a San Diego-based biotechnology company focused on the delivery of nervous system growth factors via gene transfer for the treatment of neurodegenerative disorders. Ceregene is providing CERE-110 for the study.

About Banner Sun Health Research Institute

For 23 years, Banner Sun Health Research Institute, part of nonprofit Banner Health, has been a leader nationally and internationally in the effort to find answers to disorders of aging including Alzheimer’s disease. The institute, together with its Arizona Alzheimer’s Consortium partners, has been designated by the National Institutes of Health as one of just 29 Alzheimer’s Disease Centers in the nation. The institute’s Cleo Roberts Center for Clinical Research takes laboratory discoveries to clinical trials that foster hope for new treatments. Banner Health is Arizona’s leading health care provider and second largest private employer.

Source: Banner Sun Health Research Institute

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