Alzheimer Related News Items
News as of 10/04/98
For more info on these abstracts write/call Ed Cabic (edcabic@home.net or 410-992-7197)
For more AD information, see Alzheimer Information at http://www.connext.net/~seniors/infoad.htm
Copies of these reports are posted there
This web page was started at the Florence Bain Senior Center in Columbia MD
Drugs
Zyprexa Reduces Symptoms In AD Patients - Study results show that Eli
Lilly & Co.'s Zyprexa® (olanzapine) is able to improve psychosis and behavioural
disturbances in patients with AD. The study results were presented at the
third Congress of the European Federation of Neurological Societies. Zyprexa significantly
reduced agitation, delusions and hallucinations compared to placebo, without the adverse
side-effect profile associated with other antipsychotic agents. The drug is currently
licensed for the management of schizophrenia and related psychotic disorders. Debilitating
psychosis and behavioral disturbances are often associated with AD and have a substantial
impact on quality of life for both patients and their caregivers. Approximately half of
patients seen in outpatients clinics and three quarters of those in nursing homes suffer
from significant behavioral disturbances and the incidence of psychotic symptoms can be as
high as 73 percent, with patients experiencing delusions, paranoia and hallucinations. Doctor's
Guide 9/22/98
Signal Expands Patent Position In Key Map Kinase Gene Regulation Pathways with
University of Massachusetts Licenses - Signal Pharmaceuticals announced 10/1/98
two exclusive license agreements with the University of Massachusetts Medical School
(UMMS). The UMMS licenses grant Signal rights to JNK3 knockout mice and related technology
developed jointly by Dr. Davis at UMMS and Dr. Richard Flavell at Yale University. Dr.
Davis previously reported in the journal Nature that mice engineered to be deficient in
the brain-specific JNK subtype, JNK3, are resistant to experimentally induced seizure and
associated neuronal cell death. Drugs that selectively inhibit JNK3 therefore may be
therapeutically important for treating epilepsy, as well as neurodegeneration associated
with AD, Parkinson's disease, stroke and head trauma. PR 10/1/98
New Finding Showed Vioxx Specifically Targeted Enzyme Linked to Pain While Sparing
Enzyme Believed to Protect Stomach - New study findings showed that Vioxx, a
once-a-day investigational medicine and arthritis being developed by Merck & Co
specifically blocked an enzyme known as COX-2 that is associated with producing pain and
inflamation, while sparing a second enzyme called COX-1 that is believed to be critical to
protecting the lining of the stomach. Vioxx is a member of a class of medicines called
COX-2 specific inhibitors. Phase III studies evaluating the clinical efficacy and safety
of Vioxx for the treatment of the signs and symptoms of osteoarthritis and for the relief
of pain have been completed. Studies with Vioxx are under way in rheumatoid arthritis and AD.
Additional studies are planned in colon cancer. PR 9/6/98
Cortex Receives Additional Ampakine Patent - Cortex Pharmaceuticals
announced the issuance of U.S. Patent No. 5,783,587 entitled ``Benzoyl
Piperidines/Pyrrolidines for Enhancing Synaptic Response.'' This patent is the fifth to
issue from a series of patents to protect the Ampakine family of compounds and various
medical uses of the compounds. CX516, one of Cortex's Ampakines, is currently being
investigated in two separate clinical trials at the National Institutes of Health (NIH) in
Bethesda, MD, in patients with AD and patients with schizophrenia. Cortex
has completed a preliminary human safety study with a second generation Ampakine, CX691.
This compound was designed to have a longer half life in humans, and the preliminary study
has confirmed that it does. Furthermore, in a number of animal behavior assay systems,
CX691 appears to be 50 to 100 times more potent than CX516 and has an impressive margin of
safety. These Ampakines act to increase the strength of signals at connections between
brain cells. Aberrant neural connections or loss of these connections is believed to be
responsible for the memory difficulties associated with AD and to
contribute to the memory and cognitive dysfunction seen in schizophrenia. PR 10/1/98
SIBIA Neurosciences Successfully Completes Phase I Clinical Trial With SIB-1553A;
Commences Multiple-Dose Study - They announced 9/28/98 they have
successfully completed a single-dose Phase I clinical trial with their proprietary
compound for AD, SIB-1553A, and that they will now start a multiple-dose
Phase I trial. The use of SIB-1553A is based on its selectivity for nicotinic ion channel
subtypes. PR 9/28/98
Genes & Genetic Issues
Genome Map Will Change Healthcare - Medical advances linked to the
mapping of the human genome -- the complete set of human genes -- will radically
change the healthcare process, said Dr. Francis Collins, director of the National Human
Genome Research Institute. Genetic-based diagnostic tests and therapies are the next
revolution in medicine. He noted that genome research to date has already yielded
information about gene mutations that may be linked to specific diseases, and this may
lead to screening tests for disorders such as cystic fibrosis, AD, and
various cancers. The recent genome-related discovery of a mutation linked to Parkinson's
disease may be the biggest breakthrough in Parkinson's in the past 30 years. But he said
screening tests will remain a hollow victory if no treatments are available to fight the
disease in question. ``Do you really want to know that you're going to get AD
if there's nothing that can be done?'' Reuters 9/21/98
Book Review "Scientific American Molecular Neurology (Scientific
American Introduction to Molecular Medicine.)" Edited by Joseph B. Martin. 321 pp.,
illustrated. New York, Scientific American Library, 1998. $69. ISBN 0-89454-030-0. Review
by Roger N. Rosenberg states in part -The book contains 15 chapters by 21 authors. Rudolph
Tanzi's presentation of the complex molecular genetics of AD makes explanations of the way
in which mutations of the (beta)-amyloid precursor protein gene and the presenilin genes
may lead to the neuropathological characteristics of this disease approachable and easily
digestible. The book ends with an epilogue in which the editor offers a critique of the
current state of our knowledge beyond that expressed by the authors and suggests where
research must go from here. For example, he asks how we should evaluate the recent
observation that endoplasmic- reticulum-associated binding protein moves to the inner
plasma membrane when it comes into contact with A-(beta). His message is that the study of
isolated molecular events involving (beta)-amyloid precursor protein, apolipoprotein
E-(epsilon)4, the presenilins, endoplasmic-reticulum-associated binding protein, and
others will not be adequate. Only by the study of a cascade of events in which molecular
interactions are clarified will effective therapy be found for AD. New England Journal
of Medicine 9/24/98
Alzheimer's Risk Pinned on Dad - The children of older fathers are at
greater risk of developing AD, according to new research in The New Scientist. Children
born to men in their mid to late 30s are more likely to develop the disease than those
born to men in their early 30s. The scientists suspect that the ageing process damages
DNA. People having children later in life are therefore more likely to pass on flawed
genes. There is an accumulation of environmental factors which somehow alter the genome
(genetic make-up) of the father. BBC News 9/16/98 New Scientist 9/19/98 issue
Caregivers
Panel Hears Medicare Suggestions - At a meeting Sept. 8, 1998 the
National Bipartisan Commission on the Future of Medicare heard advocates recommending
Medicare changes to consider expanding health insurance coverage for future retires.
Prescription drugs, long-terms nursing home care and more mental health services were
among the new benefits proposed. Judith Riggs of the Alzheimer's Assn. also spoke. AP
9/8/98
Therapeutic Touch Calms People with AD - At the Alzheimer's Resource
Center of Connecticut, staff learned Therapeutic Touch over a six-month period, and then
began using it on people with AD. This is a modernized version of the
ancient healing technique known as "laying on of hands." It was developed in
1975 by Delores Krieger, R.N., Ph.D., and is taught in a book "The Therapeutic Touch:
How to Use Your Hands to Help to Heal" ($8.80 in paperback from Amazon.com) The staff
noticed that many people with AD reacted positively to therapeutic touch--mostly by
relaxing. Some ceased obsessive rocking. Others unclenched their fists. Some expressed
less verbal anxiety. And many were able to sleep more peacefully. When performed properly,
therapeutic touch relaxes both the recipient and the practitioner. The staff say this dual
relaxation effect can make a positive contribution to caregivers and people with
Alzheimer's. Alzheimers.com 9/14/98 citing American Journal of Alzheimer's Disease (no
date)
Innovative Training Program for Caregiver Volunteers Revealed at Kick-off
Symposium for the UN International Year of Older Persons - The primary focus of
the community-based program is the development of an in-depth training manual. The manual
is designed to help community health and social service agencies in preparing more
volunteers to effectively assist primary caregivers of chronically ill older adults. The
training manual developed by Eisai Inc. (pronounced a-zi), a research-based pharmaceutical
company, will cover a broad range of topics, including understanding the aging process and
related health conditions and challenges; the need for sensitivity, understanding and
respect for the patient; the role of the caregiver and the role and limits of the
volunteer caregiver in the home or a supervised facility; how to work effectively with the
team of family caregivers and professional health care providers; legal and safety issues;
sources for help and where to find them; and assistance in dealing with relationships and
losses. PR 10/2/98
Testing
Blood Test May Indicate AD - In a study of 73 subjects, people with AD
have lower than average levels of a particular type of amyloid beta precursor protein
(APP) in their platelets, the cells that circulate in the blood stream that are involved
in blood clot formation. Amyloid beta is the protein found in plaques in the brains of
those with AD. The protein is derived from APP, which is found in other types of tissue,
and is in particularly high concentrations in platelets. Whether this change in
concentration will be suitable for an adjunctive diagnostic tool in AD in a large
population of patients is under investigation. Reuters 9/18/98 Archives of Neurology
1998;55:1195-1200 (Sept.).
Nymox Announces AD Urinary Test - Nymox Pharmaceutical Corp. announced a
peer-reviewed publication on the new AD7C(TM) urinary assay for AD has appeared in the
Journal of Clinical and Laboratory Analysis (September 1998; vol. 12: 285-288). The report
documents in specific detail the AD7C urine test method and results from coded, double
blind trials on 200 individuals. The results have shown that urinary AD7C is a useful
peripheral AD marker which can significantly aid the physician in the diagnosis of AD. For
people with suspicious symptoms, but who do not actually have AD, AD7C testing helps the
physician rule out AD and reassure the patient. It also helps the physician find other
causes of symptoms which are often successfully treatable such as depression, metabolic
disorders and other conditions. PR 9/17/98
Prevention
Stress Impairs Memory - Stress hormones impair memory. Stress activates
the hypothalamus, a critical structure in the brain, which signals the pituitary gland to
signal the adrenal glands to release the stress hormone, cortisol. Cortisol enters the
bloodstream and circulates into the brain where it compromises memory through a mechanism
that remains unclear. Cortisol is the memory-impairing culprit because when laboratory
animals are given drugs that prevent secretion of cortisol, they show no memory problems,
even when under severe stress. Alzheimer.com 9/29/98 citing AP
Estrogen May Help Improve Memory - Estrogen may trigger improvements in
the brain's memory function. One type of estrogen, estradiol, induces formation of
dendritic spines (nerve pathways) in a region of the brain called the hippocampus.
Hippocampal function has long been associated with the progression of AD. This finding
could help explain why estrogen replacement therapies seem to slow the progression of AD
in female patients. The estrogen may help maintain memory connections in the aging brains
of postmenopausal women, for whom hormone replacement therapy has been shown to reduce the
risk of AD. Reuters 9/15/98
Sharpen Brain to Fight Memory Loss - Dr. Eszter Boksay at NYU School of
Medicine offered some tips that may help "exercise" the brain as we age. Remain
active intellectually by reading books and magazines, doing crossword puzzles. Get regular
physical exams to see if you have a treatable cause of memory impairment. Get eye and ear
checkups because when these is impair-ment here, the brain receives less stimulation.
Avoid activities that impair cognitive functions such as excessive alcohol consumption.
Quit smoking and lower blood pressure, get plenty of exercise to help improve blood flow
to the brain and to reduce the risks of tiny strokes that can cause memory loss. Take
vitamin E as an antioxidant since it may help arrest one the processes that damage brain
cells. There is some evidence that vitamin E may help slow the progression of AD and it's
routinely used in patients with memory problems. Estrogen may have some beneficial effect
on the brain. Writing things down and making lists as well as vocally repeating new
information such as the name of a person you just met will improve your memory. Another
useful way to keep the mind alert is by making periodic changes in your life. The brain,
like other parts of the body, needs to function at full capacity. Strive to keep the brain
active. AP 9/9/98
Poor Childhood Diet Linked to AD - Poor nutrition in childhood may render
the brain more vulnerable to AD and other cognitive impairments according
to a series of mental-performance tests in a group of 3,733 elderly Japanese-American men
living in Hawaii during 1991-1993. AD was much more prevalent in the shortest group of men
(4.7%) compared with men in the tallest group (2.9%). Deficits in height linked to poor
childhood nutrition may reflect deficits in brain development. There is growing evidence
that structural and functional brain reserves, thought to develop in childhood and
adolescence, may be crucial in determining when cognitive impairment begins. Brain regions
important to the development of AD (such as the hippocampus) may be especially vulnerable
to early malnutrition. Even subtle failures in growth potential may have unknown long-term
consequences on cognitive function later in life. The positive implications of the study
is that recent advances in childhood nutrition are now helping children maximize their
physical and mental potential in many countries around the world. As height increases and
childhood development improves, the authors speculate, the prevalence of cognitive
impairment and dementia could decline in future years. Reuters 9/11/98 Pediatrics
1998;102:602-609
Cell's "Recycling" May Yield Clues to Aging - Scientists at
Johns Hopkins have identified a whirling 'dervish-like' structure within cells that helps
to recycle existing compounds into ATP, the molecule that stores the energy needed for
life. They believe the discovery could point to new methods of slowing the aging process.
The structure is an enzyme called adenosine triphosphate synthase (ATP synthase enzyme),
which makes ATP. Free-radicals, the negative byproducts of metabolism, could potentially
damage ATP synthesis at the molecular level. It is believed that the gradual accumulation
of free radical damage within cells plays a key in both disease formation and the
aging process. If ATP synthase is a site of free radical damage that could explain why we
become less energetic with age. Antioxidant compounds (including vitamins C and E) are
thought to 'mop up' free-radicals and improve cellular health. A better understanding of
the cell's energy production systems could someday help researchers develop agents that
could repair damage caused by free radicals. Now that the molecular structures (involved
in energy production) are known, researchers can pinpoint damaged regions if they occur. Reuters
9/25/98 Proc. of the National Academy of Sciences 1998;95: 11605-11070.
Antioxidants in Fruit, Vegetables Slow Brain Aging - A diet rich in
fruit and vegetables may help prevent age-related mental decline. Rats fed
antioxidant-rich strawberries and spinach had better
memories and slower declines in nerve cell functions important in movement than rats fed
standard diets. Fruit and vegetables are key sources of antioxidants, nutrients that
disarm harmful molecules called free radicals. Free radicals -- the undesirable byproducts
of various metabolic functions -- damage cells. Over time, this damage, called oxidative
damage or oxidative stress, is believed to play a leading role in certain diseases
and age-related changes. Although the body also produces antioxidants, over time,
production declines. The brain may be particularly vulnerable to the damaging effects of
free radicals because it is relatively deficient in antioxidants to begin with. Free
radical destruction is thought to be a contributing factor to the decline in memory and
motor performance seen in aging. Strawberries and spinach are high in antioxidants, and
also contain an array of "phytochemicals," or plant chemicals, that appear to
have antioxidant properties. Various tests designed to measure the animals' brain and
mental functioning showed that the rats fed diets supplemented with spinach saw the fewest
age-related declines, followed by those fed the strawberry extract. Vitamin E also helped
slow mental declines over time, but not to the same extent. It may be that foods
containing a variety of phytochemicals, including phytochemicals with antioxidant
properties, may offer greater protection than individual nutrients. Researchers plan to
investigate whether these foods can protect against or reverse mental declines associated
with age-related disorders, such as AD and Parkinson's disease.
Oxidative stress may be key factor in both, recent findings suggest. Some research
also suggests that supplemental doses of vitamin E, and ginkgo biloba, a source of
phytochemicals, might lessen the effects of AD. Reuters
10/02/98 The Journal of Neuroscience 1998; 18.
Four Factors Predict "Healthy Aging" - Middle-age men who are
not overweight, do not smoke cigarettes, and who have low blood pressure and low sugar
levels have the best chance of aging well, according to the results of a study a group of
6,500 men of Japanese ancestry in California over a 28-year period. There is now
overwhelming evidence that the majority of the health problems of the elderly can be
traced back to (risk factors that) are present in middle age. The message is basically
that if you want to prevent disease in the elderly, you have to start with young adults,
if not even young children. Reuters 10/02/98 American Journal of Public Health
1998;88:1463-1468
Other Items
AD Costs Business $33 Billion Study Finds - The Alzheimer's Association
says the disease cost society $100 billion, based on a cost of more than $40,000 to treat
an AD patient. But that figure only looks at the direct health costs of hospitalization
and other care needs. In a study on how much AD costs business, the factors are (1) time
for employees to take off to care for a relative with AD cost $7.89 billion a year; (2)
productivity costs are estimated up to two times the worker's actual compensation and they
include an inability to travel, stress on other workers, lost training opportunities and
other distractions --this totals to more $13 billion a year; (3) the costs of replacing
employees who must quit to become full time caregivers, cost to Employee Assistance
Programs, taxes and contributions to medical research. The total for all exceeds $33
billion. Reuters 9/9/98
Guilford Sees Progress on Nerve Treatment - Guilford Pharmaceuticals Inc.
said 9/25/98 it had presented new data on methods of mitigating the damage caused by
strokes and other diseases and regenerating damaged nerves. They are investigating a new
approach to treating cell degeneration that occurs after stroke, AD and
Parkinson's diseases, spinal cord injuries and head trauma, and loss of blood flow to the
heart. They are studying ways to block the body's over production of PARP, an enzyme
released during these diseases. Too much PARP can kill cells. They also announced progress
in its development with Amgen Inc in developing a treatment for rejuvenating nerve
pathways to treat the ravages of multiple sclerosis, cocaine addiction, spinal cord
injuries head trauma, and Parkinson's and AD as well as other
neurological diseases. Reuters 9/25/98
New Gladstone Institute Aims to Device Therapies for AD and Other Debilitating
Brain Diseases - The Gladstone Institute of Neurological Disease, operated by the
J. David Gladstone Institute with UC San Francisco opened Sept. 11 and it will focus
solely on advancing scientific knowledge about brain diseases --such as AD, HIV-associated
dementia and stroke. The new institute will build on a 1992 discovery by Gladstone
researchers that apolipoprotein E (apoE), a protein involved in cholesterol metabolism,
also has profound effects on the growth of nerve cells. Since then, other investigators
have found that the inheritance of certain variations of the apoE gene is a significant
risk factor for AD. PR 9/11/98
AD Rockets in Developing Countries - By the year 2020 more than 75% of
people suffering from AD will come from developing countries. This is due
to the rapid increase in the population of the elderly in these countries. The disease was
becoming more common in many countries, but China was showing the greatest increase. The
next highest growth in incidence of the disease was in Latin American countries and then
India. Estimates that there are 18 million cases of the disease worldwide now and it will
30 million by 2020. Significant increases in the number of cases would adversely affect
those countries' economies. BBC News 9/25/98
AD to Quadruple by 2047 - As the US population ages, the number of people
with AD will skyrocket, nearly quadrupling in the next 50 years, according to Dr. Ron
Brookmeyer and colleagues from Johns Hopkins in the September issue of the American
Journal of Public Health. There are more than 2 million people in the US with AD in 1997,
a figure that is expected to rise to 8.6 million by the year 2047, at which time 1 in 45
Americans will be living with the disease. Potential, but as yet unproved therapies,
include antioxidant treatment, estrogen replacement therapy and the use of non-steroidal
anti-inflammatory drugs (e.g. aspirin and ibuprofen). Interventions that could delay
disease onset even modestly would have a major public health impact. Reuters 9/9/98
American Journal of Public Health 1998;88:1137-1342
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