News reports of research into Alzheimer's disease Jan - June 2001
To search by subject, go to Alzheimer's subject index.
Return to Alzheimers main page for monthly index
There's a glossary of terms used in Alzheimer's research.
Disclaimer:
This section began as an offshoot of my
gathering of news items about memory. I am not a medical expert. My
background is in psychology. The information I have gathered here should
not be taken as providing any advice.
June 2001
Research
into the causes of Alzheimer's Disease shows that amyloid plaques
develop while the illness is taking over the brain but still not
clinically evident. Accordingly, the most common scientific belief holds
that those plaques contribute to or cause the oxidative damage and
inflammation that occur and, ultimately, destroy brain cells. Now, a
mouse-model study at the University of Pennsylvania School of Medicine
has demonstrated that oxidative damage precedes
the plaques. This finding is likely to have significant implications for
treatment. "We know Vitamin E, which is an anti-oxidant, can temporarily
slow the progression of AD for some patients. What we don't yet know is
what will happen if we suppress, reduce or delay oxidative stress over
the long run."
The study appeared in the June 15 issue of The
Journal of Neuroscience.
http://www.eurekalert.org/pub_releases/2001-06/UoPM-Psfr-1406101.htm
In a decade-long
research study following more than 300 first-degree relatives of 189
Alzheimer's patients, researchers at the University of Pittsburgh
have identified a small area of chromosome 10 that, when combined
with the previously identified APOE E4 gene, significantly increase
a person's risk of developing the disease. This combination of genes
produced a 16-fold increase in the risk of AD among first-degree
relatives. By comparison, this effect is greater than the increased
risk of lung cancer caused by smoking. These new results are
supported by independent studies of AD patients and controls from
Pittsburgh, Boston, and Bonn, Germany.
The study was reported in Molecular
Psychiatry, 6 (4), pages 413-419.
http://www.eurekalert.org/pub_releases/2001-06/MP-Ngrf-1706101.htm
May 2001
Experts reviewed more than a thousand studies to develop new
guidelines for physicians for diagnosis and treatment of
Alzheimer's. The recommendations include topics ranging from how
to recognize early signs of Alzheimer's, how to diagnose, when
medication is most effective and what types of support can
improve the quality of life for patients and caregivers.
"It's important to remember there are choices available that can
make a difference in your life or the life of your husband,
grandmother, neighbor or anyone you care about who has
Alzheimer's disease," said neurologist Steven DeKosky, MD,
co-author of the guidelines. Early diagnosis is important
because research shows current medication and care options are
most effective in people with mild to moderate Alzheimer's
disease. While Alzheimer's disease has no cure, medication can
improve quality of life and cognitive functions–including
memory, thought and reasoning– particularly among people who are
mildly to moderately affected. Regular routines and activities
such as mild exercise or walking can help with behavioral
symptoms. In addition, education and support for caregivers can
improve the well-being of both the person with Alzheimer's
disease and the caregiver.
While the comprehensive guidelines were developed for physician
use, a summary is available to help patients and their families
better understand the options to discuss with their doctor.
The guidelines are published in the May 8 issue of
Neurology, the scientific journal of the American Academy
of Neurology, and online at
www.aan.com.
http://www.eurekalert.org/pub_releases/2001-05/AAoN-Ngee-0605101.htm
The " Nun Study" has followed 678
Catholic nuns from 7 convents of the School Sisters of Notre
Dame for 15 years. The stability and similarity of their lives
makes them wonderful subjects, and the duration of the project
means that it began when many were too young to manifest
Alzheimer's or other diseases related to aging. Particularly
helpful in this regard is that the sisters were required to
write autobiographical essays when they took their vows in their
20's.
The research has shown that folic acid may help stave off
Alzheimer's disease; that small, barely perceptible strokes may
trigger some dementia; and, in an especially striking finding,
that early language ability may be linked to lower risk of
Alzheimer's because nuns who packed more ideas into the
sentences of their early autobiographies were less likely to get
Alzheimer's disease six decades later.
The latest report says nuns who expressed more positive emotions
in their autobiographies lived significantly longer — in some
cases 10 years longer — than those expressing fewer positive
emotions.
The report was published in the Journal
of Personality and Social Psychology.
http://www.nytimes.com/2001/05/07/health/07NUNS.html
An excerpt from "Aging with Grace: The School Sisters of Notre
Dame Study" by Sharon M. Reynold can be found at:
http://www.mc.uky.edu/nunnet/saints.htm
Previous studies have demonstrated the benefits of
galantamine (Reminyl™) treatment in terms of efficacy and
safety in the short-term. A recent study followed 636
Alzheimer’s patients over two years, and found that patients
receiving galantamine throughout the study maintained cognitive
benefits, while the placebo comparison group declined. Moreover,
the cognitive benefits of galantamine increased over time,
relative to the predicted rates of decline in untreated
patients.
The study was presented at the American Academy of Neurology's
53rd Annual Meeting in Philadelphia.
http://www.eurekalert.org/pub_releases/2001-05/AAoN-Gtss-0905101.htm
http://my.webmd.com/condition_center_content/alz/article/1728.79858
People with low levels of B12 or
folate may have a higher risk of developing Alzheimer's
disease. A 3-year Swedish study of 370 people 75-years-old and
older found that more than half (46 out of 78) of those
diagnosed with dementia during the timeframe of the study had
both low levels of vitamin B12 or folate and Alzheimer's type
dementia. Low vitamin B12 and folate levels have long been
observed in elderly people, and it has been theorized that this
vitamin deficiency might be tied to neurological or psychiatric
disorders. This study breaks new ground by connecting these
deficiencies with Alzheimer's disease.
Vitamins B12 and folate (a form of water-soluble vitamin B) are
found in common foods. Vitamin B12 is naturally found in animal
foods including fish, milk and milk products, eggs, meat, and
poultry. Leafy greens such as spinach and turnip greens, dry
beans and peas, fortified cereals and grain products, and some
fruits and vegetables are rich food sources of folate.
The study was reported in the May 8 issue of
Neurology, the scientific journal of the American Academy
of Neurology.
http://www.eurekalert.org/pub_releases/2001-05/AAoN-RtvB-0705101.htm
Recent studies have linked Alzheimer disease and dementia
after multiple strokes to extremely high serum
homocysteine concentrations. A survey of 1299 men and
women aged 60 and over, none of who had previously had a
stroke, found an independent relationship between very high
homocysteine levels and poor performance on cognitive tests.
The folate status of the participants was checked as folate
has been shown to significantly modify homocysteine levels.
Story recall was worse among subjects with a combination of
low folate and high homocysteine than in those whose
homocysteine levels were normal or low. Homocysteine levels
increased with age and were accompanied by a comparable
decline in folate status. The researchers found independent
associations between the highest levels of homocysteine and
poorer recall. Among subjects with the highest level of
homocysteine, the odds of passing a word delayed-recall test
were identical whether their folate status was high or low.
This study appeared in the American
Journal of Clinical Nutrition.
http://www.eurekalert.org/pub_releases/2001-04/AJoC-Hhla-2504101.htm
April 2001
A cholesterol-lowering protein produced by the body,
Apolipoprotein A-1, might be able to slow the
progression of Alzheimer's disease.
Everyone has some quantity of Apo-A, in their body. It is
produced in the small intestine and the liver and is known
to help prevent coronary heart disease. At normal levels,
the protein clears cholesterol throughout the body,
including in the brain. The scientists speculate that
boosting Apo-A levels may also help clear beta amyloid, an
important part of the Alzheimer's disease plaques that
strangle normal brain cells. Further testing is needed to
confirm the role of Apo-A in animals and its relation with
Alzheimer's, before any human trials could begin.
The findings are reported in the March 27 issue of
Biochemistry, a journal of the American Chemical
Society.
http://www.eurekalert.org/pub_releases/2001-04/ACS-Nopc-0104101.htm
Laboratory-grown human neural
stem cells, the building blocks of the brain, were
successfully transplanted for the first time into the
brains of aged rats and dramatically improved the
animals' cognitive function. The results of the study
could lay the foundation for new treatments in diseases
such as Alzheimer's and Parkinson's.
Neural cell transplant studies recently suffered a
setback when transplanted fetal cells worsened symptoms
in Parkinson's patients. However, such fetal cells are
already differentiated. Laboratory-grown stem cells are
not differentiated, allowing the host brain to take
over, dictating where the stem cells should migrate and
what types of cells they should become. As a result, the
transplanted cells became functionally integrated into
the neuronal circuitry of the host animal. Postmortem
examination of the rats' brains demonstrated that the
transplanted human brain cells had not only
differentiated and were thriving in the new environment,
but that the rats' own neuronal fibers had grown
dramatically in areas associated with spatial memory.
The findings are reported in the May 1 edition of
NeuroReport, a fully refereed online journal.
http://www.eurekalert.org/pub_releases/2001-04/UoIa-Thns-2304101.htm
In a groundbreaking procedure, physicians at the University
of California, San Diego (UCSD) School of Medicine have
surgically implanted genetically modified tissue into the brain
of an Alzheimer's patient. This launches the first phase of an
experimental gene therapy protocol
for Alzheimer's disease. The therapy delivers a natural molecule
called nerve growth factor (NGF) to the dying cells in the
brain.
If the protocol is successful, implanted cells could begin to
affect brain function in a month or two, but Tuszynski cautions
that "it may take several years to test the procedure in a large
enough number of patients to determine whether it will be useful
therapy." The therapy is not expected to cure Alzheimer's
disease, but it may restore some brain cells and alleviate
symptoms such as short-term memory loss for several years.
This research was reported in the Feb. 12 issue of
Proceedings of the National Academy of Science.
http://www.eurekalert.org/pub_releases/2001-04/UNKN-Utpf-0904101.htm
Researchers have uncovered a key piece of missing
evidence in the proof that nerve cell death in
Alzheimer's disease is caused by a failed attempt at
cell division. They have found a significant number
of brain cells in Alzheimer's patients with extra copies
of chromosomes, showing attempts at cell division in
cells that are not supposed to divide. This effort to
divide may be the cause of the nerve degeneration and
dementia in Alzheimer's disease. "It's almost as if
Alzheimer's disease were a novel form of cancer." Cancer
is characterized by uncontrolled cell division. In this
study, scientists found uncontrolled cell division,
arrested in the midst of the process, is the likely
cause of the nerve cell destruction. It is speculated
that the plaques which are a hallmark of Alzheimer's
disease brain cells trigger an inflammatory response in
the brain, and that this response brings with it
proteins that trigger cell division. This finding may
signal a new approach to the treatment of Alzheimer's,
trying to prevent signals for the inflammatory response
from reaching the cells or to prevent the cells from
responding to the signals to divide.
The paper appeared in the April 15 issue of the Journal of
Neuroscience.
http://www.eurekalert.org/pub_releases/2001-04/CWRU-Rlfc-1604101.htm
March 2001
Another drug for Alzheimer's sufferers has been approved by the FDA. Reminyl® is of the same nature as the other three medications already available( Cognex®, Aricept®, and Exelon®). These are all cholinesterase inhibitors; they interfere with the action of an enzyme that would otherwise reduce the brain's supply of acetylcholine, a chemical messenger that is essential for thought processes and nerve function.
Diagnosing
Alzheimer's disease is problematic because we have had
no definitive tests for the disease (other than
after death, by examining the brain). Recent
research suggests that two markers in cerebrospinal
fluid may indicate the presence of Alzheimers. This
is exciting not only because it would make diagnosis
easier, but because it might enable us to diagnose
it much earlier. However, to be clinically useful,
they will need to develop tests that use more
readily available fluids (such as urine).
The study appeared in the November issue of the
Annals of Neurology.
Overproduction of the
brain chemical
galanin during the early stages
of Alzheimer’s may have an negative effect on the brain and contribute to the
cognitive decline of patients, according to a study involving transgenic
(mutated) mice. The study suggests the overproduction of galanin might be a
response to the deterioration of brain cells ( people with Alzheimer's have
twice as much galanin in certain areas of the brain as peers who die of
something else). While initially galanin might be beneficial, as the disease
progresses, the overexpression of galanin may become its own problem,
contributing to cognitive decline. It seems that the memory loss that occurs
with Alzheimer's may be caused by the combination of cell death and excess
galanin. It may be that a drug that blocks galanin would slow or reverse the
mental damage caused by the disease.
This report appeared in the March 20 issue of
Proceedings of the National Academy of Sciences.
http://www.eurekalert.org/pub_releases/2001-03/RPSL-Oobc-1803101.htm
January 2001
Researchers at the National Institute of
Environmental Health Sciences have found that a
protein found in patients with Alzheimer's disease
can disrupt brain signals and therefore may
contribute to the memory losses of Alzheimer's
disease. It appears the characteristic plaques found
in the brains of Alzheimer's patients may not be the
result of the disease but a cause. It is thought
that the major protein of these plaques,
beta-amyloid peptide, binds to a receptor in the
brain, thus blocking the signals thought to be
involved in learning and memory.
The report appeared in vol. 21 of the
Journal of Neuroscience.
http://www.eurekalert.org/pub_releases/2001-01/NIoE-Ehis-0101101.htm
