Recent news from Elan on Alzheimer's Disease
NPR has devoted a fair amount of time reporting on this today.
Wednesday July 7, 1:59 pm Eastern Time
Company Press Release
SOURCE: Elan Corporation, plc
Experimental Therapy May be Useful in Treating and Preventing
Alzheimer's Disease
Elan Scientists Report in Nature Animal Data on Preventing Amyloid Plaques and Brain Pathology by Immunization
AN-1792, May be Key to a Therapeutic Vaccine against Alzheimer's Disease
DUBLIN, Ireland, July 7 /PRNewswire/ -- A form of the very peptide that triggers the deposition of amyloid plaque that overwhelms the brains of
people with Alzheimer's disease may someday be used as a treatment for this devastating disease and possibly as a vaccine to prevent it.
Researchers at Elan Corporation, plc (NYSE: ELN - news; ''Elan'') reported today in the scientific journal, Nature, that immunization with a 42 amino
acid form of the beta-amyloid peptide (AB42), called AN-1792, significantly reduced pre-existing amyloid plaque and inhibited further plaque
formation in the brains of Elan's transgenic (PDAPP) mouse model of Alzheimer's disease. Elan also reported that in another study prophylactic
immunization with AN-1792 prevented the majority of treated mice from developing virtually any amyloid plaque.
Amyloid plaque formation reduced or prevented in PDAPP mouse model of Alzheimer's disease
In the studies reported today, a group of PDAPP mice were immunized with AN-1792, at an age (six-weeks) well before these mice develop amyloid
plaque and associated brain damage. At age 13 months, the brains of the mice were compared to brains from three other groups of mice which had
been inoculated with a saline solution (control), another plaque-associated protein, (serum amyloid P component (SAP)), or left untreated.
The group treated with AN-1792 had statistically significantly less amyloid plaque and surrounding neuropathology than any of the other three groups
(p value=0.001). Virtually all of the mice treated with AN-1792 had no detectable amyloid deposits in their brains. In contrast, the groups treated with
either saline or SAP had no reduction in the progressive deposition of plaques.
In a second study, a group of 11-month old female PDAPP mice (an age when numerous amyloid plaques are already in the brain) were also treated
with AN-1792. Two parallel groups of PDAPP mice from the same litter acted as controls. Seven months later (at age 18 months), the mice that received
AN-1792 had significantly (>99%; p value=0.0002) less plaque and neuropathology than untreated mice. Moreover, compared to 12-month old
untreated mice, the 18-month old treated mice had fewer amyloid plaques, suggesting that the treatment facilitates the removal of pre-existing amyloid
plaque.
Commenting on the results, Dale Schenk, Ph.D., vice president of Neurobiology at Elan said, ''In our first study the virtual absence of plaques in the
brains of the mice treated with AN-1792 indicates that the deposition of amyloid was markedly reduced or entirely eliminated. The results suggest that
the immunization with AN-1792 prevented the deposition of beta-amyloid and/or accelerated its removal from brain tissue. In the second study, the
absence of the subsequent neuronal degenerative and related inflammatory changes that usually occur around amyloid plaque suggests that the
AN-1792 treated mice never developed the degenerative lesions associated with Alzheimer's disease.
''Should AN-1792 prove as successful in future human clinical trials as it has been in our preclinical mouse studies, we believe it will help treat a
disease that devastates millions of patients and their families,'' he added.
Elan's President and Chief Operating Officer John Groom said, ''These findings, while preliminary, are very exciting. Based on the data published
today, we expect later this year to submit an Investigational New Drug Application with the U.S. Food and Drug Administration to seek approval to
begin Phase I clinical studies to assess the safety of AN-1792 in humans.''
'Amyloid Hypothesis' leads to AN-1792 as a potential new treatment for Alzheimer's disease
From the first observations made by Dr. Alois Alzheimer in 1906, scientists have long observed the presence of many beta-amyloid plaques in the
brain tissue of people who died with Alzheimer's disease. Pathologists, who observe these plaques upon autopsy, say it looks like insoluble protein
build-up has stifled surrounding brain cells. Many Alzheimer's disease experts hypothesize that it is the presence of these plaques that leads to the
brain damage which causes the devastation of a person's memory and thinking ability (cognitive functions).
''Through the course of our research and that of our collaborators we recognized that blocking the process by which amyloid plaque develops and
accumulates in the brain might enable physicians to treat Alzheimer's disease at its source. Since amyloid plaque is essentially a brain invader, we
wondered if it could be controlled like other invasive substances -- by immunization,'' said Ivan Lieberburg, M.D., Ph.D., senior vice president of
Research at Elan.
Alzheimer's disease -- A growing healthcare problem
Alzheimer's disease is a progressive, degenerative disease of the brain. It primarily afflicts older persons and begins with symptoms such as simple
confusion and forgetfulness. Ultimately, Alzheimer's disease leads to profound dementia. Patients may undergo wrenching personality changes, and
eventually become unable to care for themselves or to be cared for outside of an institutional setting.
Approximately four million people in the U.S. have Alzheimer's disease. It affects one person in 10 over age 65, and almost half of all persons over
age 85. These are the two most rapidly growing population segments in North America, Western Europe and Japan. According to the Alzheimer's
Association the overall cost of Alzheimer's disease to families and society in the U.S. is estimated at $80-100 billion annually.
''Elan's findings are particularly important because of the significant need for therapies that can alter the course of Alzheimer's disease, something that
does not exist today. I am delighted that Elan's long commitment to research on Alzheimer's disease has lead us to this important milestone and I
congratulate the many Elan scientists involved in this breakthrough,'' commented Donal Geaney, Elan's Chairman and Chief Executive Officer.
Elan Corporation, plc is a leading worldwide specialty pharmaceutical company headquartered in Ireland, with its principal research, development,
manufacturing, and marketing facilities located in Ireland, the United States and Israel. Elan's shares trade on the New York, London and Dublin Stock
Exchanges.
The statements in this press release may include forward-looking statements that involve risks and uncertainties including, the successful completion of
preclinical and clinical studies and the difficulty of predicting regulatory approvals, as well as the other risks and uncertainties detailed from time to time
in periodic reports, including Elan's annual report on Form 20-F for the year ended December 31, 1998, filed with the Securities and Exchange
Commission. Actual results may differ from the forward-looking statements.
SOURCE: Elan Corporation, plc |
