My Mom died this afternoon at 2 PM
My sister and I were fortunate enough to be with her when she stepped fully into the afterlife
We noticed her hands becoming cool and her skin color changing. Her breathing became shallower and shallower, and I knew she was on her way. She took a last breath and was gone.
Wednesday, April 30, 2008
The stamp is quite handsome as you can see.
Risky investments and rising prices seem to be everywhere these days
For the past year, branches have been selling “The Forever Stamp” for 41 cents each
“The stamp will be good for mailing one-ounce First-Class letters anytime in the future — regardless of price changes,” the agency promises.
As the penny increase of May 12 nears, the forever deal is proving irresistible to millions of Americans, according to today’s news release:
In the past several weeks, Postal Service customers have been buying Forever Stamps at a rate of about 30 million per day, bringing the amount sold to more than 6 billion since they were first offered.
The Associated Press further detailed the climb, reporting forever stamp sales of $267,696,023 in March, $207,900,132 in February and $115,303,031 in January
Monday, April 28, 2008
The mechanism of action of CTS-21166 centers around inhibiting one of the enzymes (beta-secretase) that clips off a part of a larger protein [APP] to form amyloid-beta, which comprises the plaques found in the brains of Alzheimer’s patients.
Astellas Pharma, Inc. (ALPMF.PK) and CoMentis, Inc. announced Friday that the companies have entered into an agreement to develop products from CoMentis’ beta-secretase inhibitor program, including the recently initiated, phase 2, lead candidate compound CTS-21166, an oral beta-secretase inhibitor for the treatment of Alzheimer’s disease. The agreement also includes a research collaboration to develop additional beta-secretase inhibitors.
Upon closing, CoMentis will receive an upfront payment of $80 million and an equity investment of $20 million. CoMentis has the opportunity to receive up to $660 million in development milestones and may also receive performance-based commercialization milestones. In addition, CoMentis has the right to receive development milestones for next-generation beta-secretase inhibitors discovered under the terms of the research collaboration. Astellas will fund 100% of the pre-Phase III global development costs and CoMentis will share the Phase III development costs. Astellas has exclusive worldwide commercialization rights while CoMentis retains the right to co-promote in the U.S., where profit will be shared. CoMentis will receive royalties on sales outside the U.S.
Not a bad day for CoMentis; $100M upfront is a nice chunk of change for any program, let alone one that barely cleared phase I and showed no cognitive improvements (they weren’t measured, go figure). The mechanism of action of CTS-21166 centers around inhibiting one of the enzymes (beta-secretase) that clips off a part of a larger protein [APP] to form amyloid-beta, which comprises the plaques found in the brains of Alzheimer’s patients. It is thought by reducing the amount of amyloid, the disease course may be reversed or, at least slowed; a treatment outcome that is not currently possible. There is a sort of chicken and egg game over the origin of these plaques in Alzheimer’s. Some believe the formation of these plaques is the origin of Alzheimer’s and others take the opposite tack saying the disease itself creates the plaque.
There is controversy however, as Derek Lowe points out on his blog In The Pipeline. A one year old PNAS paper shows that mice which over express APP but lack beta-secretase, actually do worse on cognitive tests than mice that only over express APP. In the clinical realm, bapineuzumab, a mAb targeting amyloid-beta from Wyeth (WYE) and Elan (ELN), is currently in phase 2 and 3 and has yet to release any data including the all important ADAS-Cog score. If these therapies do not reverse the cognition score (as measured by ADAS-Cog) the FDA might not approve them regardless.
Alzheimer's is a tough disease and eventually, given enough shots on goal, one or two will go in. If bapineuzumab is successful, CTS-21166, would potentially have an advantage long term due to the oral (or so they say, the ph1 was IV) dosing and I’m sure the BD people at CoMentis delightfully highlighted that fact. This proof of concept for the mechanism of action will come mid to late ‘08 when Wyeth releases results of the extended phase 2 of bapineuzumab. I’ll be keeping my eyes peeled.
Tuesday, April 22, 2008
Tackle the challenges of caregiving with this free football style "playbook" by Frank Broyles, former coach and Athletic Director of the University of Arkansas Razorbacks. The Playbook is an engaging, how-to guide written for those who care for someone with Alzheimer's. Coach Broyles cared for his late wife Barbara, who had Alzheimer's disease.
“My wife Betty is in the early stages of Alzheimer's. The minute I received the ‘Playbook,’ I sat down and read it word for word. What a huge blessing for me to find a straight forward, 'been there’ account of what lies ahead.
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Bob DeMarco is the editor of the Alzheimer's Reading Room and an Alzheimer's caregiver. The Alzheimer's Reading Room is the number one website on the Internet for news, advice, and insight into Alzheimer's disease. Bob has written more than 800 articles with more than 18,000 links on the Internet. Bob resides in Delray Beach, FL.
Original content Bob DeMarco, Alzheimer's Reading Room
Friday, April 18, 2008
In March, one of 59 patients enrolled in studies in Europe and the U.S. was hospitalized after developing skin lesions on the fingers and toes.
The patient developed side effects in March, was hospitalized and later released. A Wyeth spokesman told the Health Blog the patient is still being evaluated.
The FDA put a halt on the U.S. trial and and the companies voluntarily stopped the European trial,
ACC-001 isn’t related to bapineuzumab, an antibody against Alzheimer’s plaques now in phase III testing.
Work on an earlier vaccine, called AN-1792, was stopped by the companies years ago after some patients in a clinical trial developed encephalitis.
Study Results Of GAMMAGARD S/D And GAMMAGARD LIQUID In Patients With Mild To Moderate Alzheimer's Disease Announced
The study met the primary endpoint criteria favoring
The study also met
Results show findings
Beta-amyloid is a
Results From Largest Statin Study Of Patients With Alzheimer's Disease Show Lipitor(R) Has No Significant Impact On Disease
In a study in patients with mild-to-moderate Alzheimer's disease (AD), the addition of Lipitor (atorvastatin calcium tablets) 80 mg to Aricept® (donepezil HCl) 10 mg showed no significant differences in cognition or global function (key measures of Alzheimer's progression) compared to placebo plus Aricept 10 mg. Furthermore, no statistically significant differences were seen on various cognitive, behavioral and functional secondary endpoints. However, the Lipitor arm was not associated with greater cognitive decline than the placebo arm in this trial. The results were presented today at the annual American Academy of Neurology meeting in Chicago.
Antioxidant Therapy Shows Early Promise Against Alzheimer's Disease - Improved Blood Flow Boosted Cognition And Behavior In Mice With AD-Like Illn
For the first time, new research demonstrates that curbing harmful antioxidant processes in the brain's vasculature can reverse some of the cognitive decline associated with Alzheimer's disease.
findings published in a recent issue of the Proceedings of the National Academy of Sciences.
Alzheimer's Reading Room
Several years ago I refused to allow my mother to be medicated with depression drugs. Instead, I decided to work very closely with her to try to bring her out of her "funk". Exercise, a good diet, lots of patience and fostering a "secure environment" worked.
Later I discussed my mother's incontinence with her doctor. He told me he could "prescribe" something. With Alzheimer's as a variable in the equation I decided against it. I tired to get my mother to visit the toilet as often as possible. While this was very trying and difficult, I was eventually able to get her into a pattern of going even when she did not feel it was necessary.
It takes lots of patience and perseverance to accomplish these goals. I am not saying its easy. I do believe its possible to improve situations if you can get a new pattern of behavior established.
I did get lots of communication tips from The Validation Breakthrough: Simple Techniques for Communicating with People with 'Alzheimer's-Type Dementia'
Thursday, April 17, 2008
Professor delivers 'Lecture': Randy Pausch's The Last Lecture makes its debut at No. 2 on USA TODAY's Best-selling Books list, but Pausch, who is dying of pancreatic cancer, says sales aren't the reason he wrote the book.
"I personally only cared about the first three copies, which are for my kids," he says. The book, written with Wall Street Journal columnist Jeff Zaslow, builds on a "last lecture" Pausch gave in September at Carnegie Mellon. Many in the publishing world believe Lecture will be the next Tuesdays With Morrie, which became a publishing sensation. It, too, dealt with wisdom imparted by a dying professor. Hyperion has had nine printings; 2 million copies are in print.
GALLERY: Pausch's life in photos
The study involving 9,752 people in northern California found that those with high cholesterol levels between ages 40 and 45 were about 50 percent more likely than those with low cholesterol levels to later develop Alzheimer's disease.
The findings were presented on Wednesday at a meeting of the American Academy of Neurology in Chicago.
Wednesday, April 16, 2008
For a more detailed report on early-onset Alzheimer's, visit the U.S. Administration on Aging.
HealthDay News -- The root cause of early-onset dementia is usually not Alzheimer's, but rather another neurodegenerative or autoimmune disorder, new research suggests.
The study authors acknowledge that -- age aside -- the most common forms of dementia are Alzheimer's disease, vascular dementia and the brain damage-associated condition known as Lewy body dementia. However, their current work indicates that among patients below the age of 45, the problem is much more likely to be traced back to diseases such as multiple sclerosis, Huntington's, lupus or HIV infection, among others.
"This is really a novel finding, because there hasn't really been a study that's looked at young-onset dementia in this way," said study author Dr. Brendan J. Kelley, a neurologist at the Mayo Clinic in Rochester, Minn. "And the message is that young-onset dementia is generally not related to Alzheimer's."
The work of Kelley and his team was expected to be presented April 15 at the American Academy of Neurology annual meeting, in Chicago.
The U.S. Administration on Aging highlights 2006 estimates released by the Alzheimer's Association, which indicate that between 220,000 and 640,000 American men and women currently suffer from early-onset dementia. The association specifically defines "early-onset Alzheimer's" as referring to cases that develop before the age of 65.
However, in their study, Kelley and his team focused exclusively on 235 patients diagnosed with a form of dementia diagnosed between the ages of 17 and 45 -- citing statistics suggesting that 12 in 100,000 people develop some form of early-onset dementia before the age of 45.
All the study patients had sought care at the Mayo Clinic between 1996 and 2006, and all had normal cognitive function prior to their dementia diagnosis.
A medical record analysis revealed that despite the fact that most adult dementia is a function of Alzheimer's, less than 2 percent of the cases among the under-45 group was attributable to that disease.
Kelley and his colleagues found that other neurodegenerative conditions -- such as frontotemporal dementia, a group of diseases commonly misdiagnosed as Alzheimer's -- were at play in almost one-third of the cases.
Autoimmune and inflammatory disorders -- such as MS -- accounted for just over 20 percent of the dementia cases. Metabolic abnormalities were cited in just over 10 percent of the diagnoses, while for another 20 percent, no cause for dementia could be established.
Kelley said his work is ongoing. And he added that he and his colleagues are now trying to identify specific disease markers for early-onset dementia to help physicians distinguish those cases prompted by causes other than Alzheimer's.
"Because some of the other disorders linked to early dementia have treatable profiles that allow targeting not just of the symptoms but of the underlying disease process," he noted. "So, we really should be looking to identify them quickly when they are the cause, because the research suggests that treatment could result in a direct improvement of the patient's cognition and behavior."
Greg M. Cole, associate director of the Alzheimer's Disease Research Center at the UCLA David Geffen School of Medicine, described the findings as "interesting, but not completely unexpected".
"We know that Alzheimer's gets rarer and rarer the younger you go," he said. "So, when you're focused as this study is on people between 17 and 45 -- really before middle-age -- it's more likely you'll find some other cause for the dementia, which can be a variety of different things."
"But if you're looking at these other autoimmune causes -- multiple sclerosis, lupus, HIV -- the real question is, can you treat any of this?," pondered Cole. "Because you can get lupus and MS to go into remission. So, in this case, if patients are getting dementia caused by either disease, can the dementia also go into remission? If they can get that to happen, that would be very interesting."
For additional information on early-onset Alzheimer's, visit the U.S. Administration on Aging.
Scientists may have learned why some people retain sharp minds and clear memories despite having the so-called brain plaques and tangles that are the hallmarks of Alzheimer's disease.
comparing the brains of these people to others who had all the memory-robbing symptoms of Alzheimer's, the researchers said on Tuesday they found those who avoided dementia consistently had a larger part of the brain called the hippocampus.
Dr. Deniz Erten-Lyons of Oregon Health and Science University in Portland, who led the study
said the findings could inspire new ideas for combating Alzheimer's disease, the most common form of dementia in the elderly.
I think one of the important things of our study was emphasizing that there's other things that we need to focus on as well — other mechanisms that we don't know and do play a role in Alzheimer's disease
The changes associated with Alzheimer's disease usually begin in the hippocampus,
That's where the brain shrinkage starts in Alzheimer's disease
Tuesday, April 15, 2008
Baxter and The Alzheimer's Disease Cooperative Study (ADCS) group announced a decision to pursue a multi-center U.S. Phase III study evaluating the role of GAMMAGARD. The study design is undergoing review with the U.S. Food and Drug Administration with the intention of initiating patient recruitment later in 2008. The trial is expected to include approximately 35 leading academic centers in the United States that are members of ADCS.
Study Suggests GAMMAGARD LIQUID May Target the Primary Pathway Involved in Alzheimer's Disease
Laboratory study shows naturally occurring antibodies contained in GAMMAGARD LIQUID may bind to the primary culprit for Alzheimer’s disease
The University of Tennessee Health Science Center and Baxter International Inc. (NYSE: BAX) today announced data from a laboratory study demonstrating natural antibodies contained in GAMMAGARD LIQUID [Immune Globulin Intravenous (Human)] (IGIV), marketed as KIOVIG in the European Union, a
plasma-derived antibody replacement therapy indicated for primary immunodeficiency
disorders and being studied in Alzheimer’s disease, binds directly to multiple aggregated, or clustered, forms of the beta-amyloid peptide molecule. The beta-amyloid molecule may contribute to beta-amyloid plaques, which are thought to be the primaryculprit causing Alzheimer’s disease. The results of this in vitro (laboratory) study were presented by Dr. Brian O’Nuallain, assistant professor, UT Medical Center, Knoxville, University of Tennessee Health Science Center at the American Academy of Neurology (AAN) Annual Meeting.
Previous clinical studies suggest that antibody-based immunotherapy may boost the body’s own immune response to reduce beta-amyloid, the protein responsible for plaque formation commonly found in the brains of Alzheimer’s disease patients. In addition, recent laboratory research suggests that specific forms of beta-amyloid –oligomers and fibrils that are aggregates or clusters of beta-amyloid – may be toxic to the neurological system and lead to the progression of Alzheimer’s disease. “IGIV therapy may contain antibodies that possibly have strong binding characteristics to several aggregated forms of the beta-amyloid peptide that are believed to cause Alzheimer’s disease,” said Dr. O’Nuallain. "These initial findings could be promising in Alzheimer's disease research using naturally occurring antibodies."
The oral presentation at AAN, entitled “Affinity Isolation and Characterization of
Abeta Conformer-Reactive Antibodies Contained in Human Immune Globulin (IVIG),”
showed that GAMMAGARD contains naturally occurring antibodies that directly bind to
different forms of beta-amyloid protein, including oligomers and fibrils.
“Observations from this study provide insight into how GAMMAGARD LIQUID
may be of potential clinical benefit for Alzheimer’s patients,” said Dave Morgan, director of Neuroscience Research, University of South Florida. “This study suggests that GAMMAGARD LIQUID may target the primary pathway involved in Alzheimer’s disease and justifies additional studies to evaluate whether GAMMAGARD LIQUID can effectively reverse the effects of Alzheimer’s disease.”
According to the Alzheimer’s Association, an estimated 5.2 million Americans
have Alzheimer’s disease, including one out of eight people age 65 and older, and the
number of new cases per year is expected to grow to 454,000 by 2010. No cure
currently exists that can halt or delay the brain deterioration associated with Alzheimer’s disease, but new research shows encouraging results. The study’s findings showed how the mechanism of action of GAMMAGARD may work on multiple forms of the beta amyloid peptide to protect the human brain from dementia and may facilitate the development of treatment for patients with Alzheimer’s disease.
Additional GAMMAGARD Trials in Alzheimer’s Disease
At the AAN meeting, other studies will be presented on the use of GAMMAGARD in Alzheimer’s disease. One oral presentation scheduled for April 17 – “A Double-Blind, Placebo-Controlled, Phase II Clinical Trial of Intravenous Immunoglobulin (IVIG) for Treatment of Alzheimer’s Disease” – will discuss the evaluation of the efficacy, tolerability and safety of GAMMAGARD in the treatment of mild to moderate stage Alzheimer’s disease.
The oral presentation, “Intravenous Immunoglobulin Increases Brain Glucose
Metabolism in Alzheimer Disease,” will also be presented on April 17 and will discuss
the analysis of brain activity using imaging data. The brain metabolism results were
based on serial Positron Emission Tomography (PET) scans, an imaging technique
sometimes used in the diagnosis of Alzheimer’s disease. Further, Baxter and The Alzheimer’s Disease Cooperative Study (ADCS) group announced a decision to pursue a multi-center U.S. Phase III study evaluating the role of GAMMAGARD. The study design is undergoing review with the U.S. Food and Drug Administration with the intention of initiating patient recruitment later in 2008. The trial is expected to include approximately 35 leading academic centers in the United States that are members of ADCS.
Original content Bob DeMarco, the Alzheimer's Reading Room
A University of Iowa researcher is conducting an Internet-based study to see if writing about their thoughts and feelings about care-giving can be a strategy to help those family caregivers reduce their stress.
10 Million Baby Boomers will get Alzheimer's - 1 Million in California
Journalists are invited to cover this largest such Alzheimer’s event, both locally – at points around California for scheduled departure points, and at the State Capitol. Rally Participants (currently 1,415 registered) will include: People with Alzheimer’s, family members, friends and neighbors, caregivers, health care professionals and science researchers. Alzheimer’s Rally on the Capitol Steps (North Side, L Street), Wednesday, April 16, 2008, 12:30pm to 2:00pm (11:30am attendees check-in).
Around California – Wednesday morning, April 16, Californians will be gathering, to fly and to take buses.
To cover the story from these perspectives, including interviews with participants, please see the list of Media Contacts for the Alzheimer’s Association throughout California.
Rally Program – Includes:
* The Face of Alzheimer’s by two Persons with Alzheimer’s;
* Alzheimer’s philanthropist Elizabeth Gelfand Stearns;
* Family Caregivers (including a 14-year-old helping care for her father with Alzheimer’s); legislators on Alzheimer’s;
* Actress/singer/director and long-time Alzheimer’s Champion Lea Thompson;
* Advocates – from throughout the Alzheimer’s journey, coming from throughout California.
12:15 Group Photo of California Legislators on the Capitol Steps, surrounding by Alzheimer’s Advocates (all California Assemblypersons and Senators invited). Group Photo to be made available immediately following the Rally.
12:30 – 2:00 pm Rally Program
Media Bull Pen – Available to assist all attending journalists. This area will be clearly marked as “News Media” near the stage/Capitol Steps.
Miss California 2007, Melissa Chaty, will be among those available for interviews. Appearing on the Rally Program, she is a long-time Alzheimer’s volunteer and has made “Alzheimer’s Advocacy and Awareness” her platform, in honor of her grandfather. Photo available: Media Contact Brad Makaiau.
Available materials will include the new two-page “Preliminary Findings: 2008 California Data Report on Alzheimer’s Disease” which includes these highlights:
* Alzheimer’s in California will double within the next generation.
* Every year over 11,000 Californians will develop the disease.
* One in eight California Baby Boomers will have Alzheimer disease.
* Chart: Summary of Alzheimer’s by Race/Ethnicity Percentage Increase from 2008-2030. Alzheimer’s does not discriminate. Every ethnic group will have a significant increase.
* Chart of Every California County: Number and Percentage Increase in People 55+ with Alzheimer’s, for 2008 and 2030, noting the % increase by county. Most counties will see at least a doubling in Alzheimer’s disease.
* Chart: Estimated Per Person Medi-Cal Costs in California (2007)
* The complete County-by-County 2008 California Data Report on Alzheimer’s Disease – publishing in June 2008 – is being prepared by the Institute for Health & Aging, University of California, San Francisco. The Report is being made possible by a grant from The Rosalinde and Arthur Gilbert Foundation.
To receive a fax or e-mail copy of the Preliminary Report, see the Media Contacts list provided below.
Media Contacts – Alzheimer’s Association, California:
Jill Center, Northern California, 650-962-8111; Cell: 415-730-5958, Jill.Center@alz.org
California Southland (Los Angeles, Riverside & San Bernardino Counties):
Barbara Goen, 323-930-6265; Cell: 213-910-1949, Barbara.Goen@alz.org,
or Akila Gibbs, 323-930-6255; cell: 323-646-6834, Akila.Gibbs@alz.org
Jim McAleer, Orange County, 949-955-9000, Jim.McAleer@alz.org
Brad Makaiau, San Diego/Imperial Co, 858-492-4400; Cell: 619-865-7556, Brad.Makaiau@alz.org
Catherine Remak, Santa Barbara/Central Coast, 805-892-4259, Cremak@centralcoastalz.org
From March 13, 2008 Announcement of Rally by the Alzheimer’s Association:
As the Alzheimer’s epidemic continues upward, wreaking havoc for increasing numbers of California families, the Alzheimer’s Association projects that the state’s already overwhelmed care and research infrastructure will shrink – and in some cases disappear – if Sacramento lawmakers complete proposed mid-year budget cuts. To shine a spotlight on what has been described as “the public health crisis of the 21st Century,” the five California chapters of the Alzheimer’s Association, and its Sacramento-based California Council, today announced that volunteers and staff are organizing over 1,000 individuals from throughout California to turn up in Sacramento for a first-ever Alzheimer’s Rally on the Capitol Steps (North Side, L Street), Wednesday, April 16, 2008, 12:30pm to 2:00pm (11:30am attendees check-in).
Alarmed that California is headed in the wrong direction when it comes to one of the top fears among Baby Boomers and the aging American population, Alzheimer’s Association Advocates from every part of the state will stand on the steps of the state capitol and tell their elected representatives – some of whom are expected to attend – that when it comes to Alzheimer’s: “The present is catastrophic and California’s totally unprepared for what’s coming.” Coming to Sacramento, by plane, train, bus and automobile, in a pure exercise of representative democracy, they’ll ask their public servants, when it comes to Alzheimer’s and related dementias: “What’s your plan?”
Among those also expected to participate are representatives from the California Alzheimer’s infrastructure that is now at risk, including: Alzheimer’s Day Care Resource Centers, Adult Day Health Care, Caregiver Resource Centers, In-Home Supportive Services, physicians and other Home Health Community Providers, and those representing Medi-Cal Optional Benefits.
California’s Alzheimer’s Research Centers (ARCCs) are now also facing cuts that would: slow current research, delay better diagnosis, treatment and management strategies for Alzheimer’s, and impact dementia care in other health settings. The ten California ARCCs are at: UCSF, UCSF at Fresno, UC Davis, UC Davis at Martinez, Stanford, UCLA, USC, USC Rancho Los Amigos Rehabilitation Center, UC Irvine and UC San Diego.
William Fisher, Alzheimer’s Association CEO for Northern California, said there currently are over 5 million Americans with Alzheimer’s or a related disorder – 500,000 here in California. If no cure is found, those numbers could triple by mid-century, to 16 million Americans. Meanwhile, Alzheimer’s can be expected to bankrupt the health care system. Already, annual National costs of care (direct and indirect) for individuals with Alzheimer’s are at least $100 billion; current costs to American businesses are $61 billion. One out of every eight people age 65 and older has Alzheimer’s and nearly one out of every two over age 85 has it. Alzheimer’s is the seventh leading cause of death in the United States.
According to Peter Braun, President and CEO of the California Southland Chapter, seven out of 10 people with Alzheimer’s live at home, where family and friends provide almost 75% of their care. However, crucial at-home care will decline as an option if the State continues to pull back on what little infrastructure there currently is to support families, by: under-funding community providers, forcing the closure of adult day health care programs, and reducing access to physicians. Fisher said that in addition to the immediate pull-backs in the State’s community support apparatus – limited though it already is for the exploding Alzheimer’s population – one of the most significant demands of Alzheimer’s caregivers and others throughout the state is the failure to plan ahead. “California must create a strategic planning process in order to be ready for the Alzheimer’s epidemic.” He said, “To not be ready for a public health crisis that we already know is forming would be unconscionable.”
Braun succinctly summarized the situation this way: “Alzheimer’s is surging forward, and, at this moment, California is falling backward.”
Loretta Redd, Alzheimer’s Association Executive Director for Santa Barbara and the Central Coast, said, “These cuts are a blow to a fragile network of services families use to help them keep their Alzheimer’s patient at home, for perhaps years, rather than placed in far more costly institutions.”
Jim McAleer, Alzheimer’s Association Executive Director for Orange County, said that if California were to travel down this path, “The message from the California State Legislature, to all Californians – because every Californian is vulnerable to Alzheimer’s – would be: ‘If you’re struck by Alzheimer’s, you and your family are on your own.’” In fact, McAleer said, “These proposed cuts from the developing state budget situation sabotage smart, cost-saving mechanisms, such as aging-in-place and community-based care.” Ultimately, he said they do not help save California’s budget situation, and, “as an assault on family caregivers, they are unacceptable.”
Lisa Bruner, Interim CEO for the Alzheimer’s Association in San Diego County, said the message Alzheimer’s families and other Advocates will carry to legislators is personal as well as public: “If you do not think you know a person with Alzheimer’s, you certainly will.” She said, “Now is the time to address this escalating epidemic.”
NOTE to Journalists: The Alzheimer’s Association can assist you in developing local-to-capital “Ms .and Mr. Smith Go to Sacramento” stories. Photography from the Alzheimer’s Association will be available from the April 16 Rally.
Alzheimer's Association, California:
Jill Center, Northern California, 650-962-8111
California Southland (Los Angeles, Riverside &
San Bernardino Counties):
Barbara Goen, 323-930-6265
Akila Gibbs, 323-930-6255
Jim McAleer, Orange County, 949-955-9000
Brad Makaiau, San Diego/Imperial Co, 858-492-4400
Catherine Remak, Santa Barbara/Central Coast,
Saturday, April 12, 2008
Dr. Murali Doraiswamy and social worker Lisa Gwyther of Duke University have almost 40 years of combined experience working with and caring for Alzheimer’s patients and their families. Their new book, "The Alzheimer’s Action Plan," was written to answer many of the questions they have received about diagnosis and treatment.
“Alzheimer’s is a very complex disease, so the more people know, and the more they know about how to approach this issue, the more in control they’ll feel and the less frightening it’ll be,” said Gwyther.
It also presents some hard facts about mistakes that are often made by healthcare professionals, whom Doraiswamy said often have varying levels of understanding of the disease.