Alzheimer's Images
Alzheimer’s
disease (AD) is a progressive, degenerative disease of the brain that causes a
person to forget recent events and familiar tasks. The most common form of
dementia, AD is relentless, interfering with daily functioning and eventually
leading to death. At this time, there is no clear understanding of how the
disease develops, and there is no medical treatment available to stop the
progression of the disease. However, suspected causes include genetic
predisposition, abnormal protein buildup in the brain, and environmental toxins.
Current research has shown that
there are two distinct differences in the brains of AD patients when compared
with non-AD patients. First, there is the formation of senile plaques that
disrupt the normal structure and function of nerve cells, but it is unknown
whether these plaques are the cause or an effect of the disease. Second, there
is the formation of neurofibrillary protein tangles that cause the branches that
sprout from neurons to become disorganized and collapse. This lack of structure
results in severed neuronal connections that cause the dementia and brain-cell
death associated with AD.
Dr.
Wayne Schultz is
initiating a new project to study two enzymes, tau and GSK3b, that form tangles.
These enzymes normally create a network of biochemical signals that regulate the
structure of brain cells. They are responsible for maintaining the connections
between brain cells that allow the transfer of messages. For an unknown reason,
changes in these enzymes lead to AD. By carefully examining the structures of
these enzymes, we can begin to understand how they interact and may discover why
they often function abnormally in older people. This structural information may
also be useful when designing novel treatments for AD.
WARNING: READING SCROLLDOWN COULD CAUSE DEMENTIA
A
recent study
in the journal Neurology says that “lowbrow” jobs increase a person’s
chances of acquiring Alzheimer. Three conclusions can be made from a study like
this. The first and most obvious is that using your brain, especially from one's
thirties and on as the study suggests, prevents the plaque
build up on one's noodle. That is the use it or loss it hypothesis. The next
is people predisposed to Alzheimer could avoid mental challenging professions.
And finally people that use their noodle more typically are richer and more
health conscious than folks who do not.
Scanning for Alzheimer’s Disease
Norm Foster
Photo: Gregory Fox |
Alzheimer’s is a disease that takes a terrible toll on the memories and
lives of millions of adults and their families each year. Unfortunately, there
is no definitive test for Alzheimer’s disease, and other disorders can mimic
its symptoms. New drugs and therapies can slow the spiral of memory loss and
behavior changes in Alzheimer’s patients, but they work best if the disease is
diagnosed and treated early.
U-M neurologists, working with researchers at three other universities, are
evaluating positron emission tomography, or PET scanning, as a diagnostic aid in
Alzheimer’s disease. Norman Foster, M.D., who leads the research team, says
initial results from the study show PET scanning can help physicians
differentiate Alzheimer’s disease from other neurodegenerative disorders.
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PET scans showing glucose metabolism in the brain.
The color scale at the bottom indicates how glucose metabolism is
measured in the scans. The first row (REF) shows the brain as it is
oriented in the PET scans below. The second row (NL) shows a
“normal”elderly subject, the third row (AD) a patient with
Alzheimer’s disease, and the fourth row (FTD) a patient with
frontotemporal dementia.
Courtesy of Norm Foster
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PET scans show activity in different parts of the brain and how each part is
reacting to disease. Brain activity — or the lack of it — is what matters in
Alzheimer’s disease, says Foster, a professor in the Department of Neurology
in the U-M Medical School. Foster directs the Cognitive Disorders Clinic in the
U-M Geriatrics Center and is the associate director of the Michigan
Alzheimer’s Disease Research Center. He is also a senior research scientist at
the U-M Institute of Gerontology.
Researchers have tried other medical imaging techniques to detect the
disease, with disappointing results. Magnetic resonance imaging (MRI) and
computed tomography (CT) scans can rule out other disorders, but they can’t
positively detect Alzheimer’s. Based on the U-M study and other evidence,
Foster feels that early diagnostic testing with PET could become common practice
within a few years, and will help physicians choose the best treatment for their
patients.
“In some cases, memory loss isn’t the first symptom,” says Foster.
“It could be behavioral or language changes, or difficulty with everyday
activities. All symptoms can be caused by different conditions requiring
different kinds of treatments and may or may not respond to the same
medications.
“PET imaging has a great advantage because it shows specific patterns of
brain activity, which differ in normal aging, Alzheimer’s disease and other
kinds of dementia. And we understand from PET scans which parts of the brain are
most damaged in different disorders and how these changes relate to patients’
symptoms.”
Other universities participating in the study are the University of
California-Davis, the University of Pennsylvania and the University of
Washington. Funding was provided by the National Alzheimer’s Coordinating
Center, part of the National Institute on Aging.
http://www.kellysalerno.com/theforgetting/videolinks.html
The Forgetting – A Portrait of Alzheimer's
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- Copy the HTML CODE to the right of your selection.
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| Normally, the A2M protein protects against
Alzheimer's by delivering A-beta into the neuron where it is
degraded. However, to enter the neuron by the LRP receptor, the A2MA-beta
complex must first bind a protease. Tanzi speculates that while the
A2M-2 gene is capable of making normal protein, it might produce
some fraction that is unable to bind protease. With entry into the
neuron impeded, A-beta could accumulate in the extracellular spaces,
eventually forming destructive Alzheimer's plaques. ApoE may hasten
the disease process by competing with A2M-2 for LRP and A-beta. |
Alzheimer's Disease
Alzheimer's
Disease Wikipedia
"Alzheimer's disease" is the term used to describe a dementing
disorder marked by certain brain changes, regardless of the age of onset.
Alzheimer's disease is not a normal part of aging--it is not something that
inevitably happens in later life. Rather, it is one of the dementing
disorders, a group of brain diseases that lead to the loss of mental and
physical functions.
The disorder, whose cause is unknown, affects a small but significant
percentage of older Americans. A very small minority of Alzheimer's patients
are under 50 years of age. Most are over 65.
Alzheimer's disease is the exception, rather than the rule, in old age.
Only 5 to 6 percent of older people are afflicted by Alzheimer's disease or
a related dementia--but this means approximately 3 to 4 million Americans
have one of these debilitating disorders.
Research indicates that 1 percent of the population aged 65-74 has severe
dementia, increasing to 7 percent of those aged 75-84 and to 25 percent of
those 85 or older. At least half the people in U.S. nursing homes have
Alzheimer's disease or a related disorder; in 1985, the annual cost of
caring for individuals with Alzheimer's disease and related dementias in
institutional and community settings was estimated between $24 billion and
$48 billion for direct costs alone and is probably higher today. As our
population ages and the number of Alzheimer's patients increases, costs of
care will rise as well.
Although Alzheimer's disease is not curable or reversible, there are ways
to alleviate symptoms and suffering and to assist families. Not every person
with this illness must necessarily move to a nursing home.
Many thousands of patients--especially those in the early stages of the
disease--are cared for by their families in the community. Indeed, one of
the most important aspects of medical management is family education and
family support services. When, or whether, to transfer a patient to a
nursing home is a decision to be carefully considered by the family.
Article
Continued...
NEWS ARTICLES
Researchers
isolate Alzheimer's fighting gene December 2003 - Ananaova
Alzheimer's
abnormal brain proteins glow September 2003 - Nature
Alzheimer's
linked to magnets in brain UPI - April 2003
HEALTH INDEX
ALPHABETICAL INDEX
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CRYSTALINKS MAIN PAGE
How the Brain and Nerve Cells Change
During Alzheimer's Disease
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One of the hallmarks of Alzheimer's
disease is the accumulation of amyloid plaques between
nerve cells (neurons) in the brain. Amyloid is a general
term for protein fragments that the body produces normally. Beta-amyloid
is a fragment of a protein that is snipped from another protein
called amyloid precursor protein (APP). In a healthy brain, these
protein fragments would be broken down and eliminated. In
Alzheimer's disease, the fragments accumulate to form hard,
insoluble plaques.
Neurofibrillary tangles consist
of insoluble twisted fibers that are found inside of the
brain's cells. They primarily consist of a protein called tau, which
forms part of a structure called a microtubule.
The microtubule helps transport nutrients and other important
substances from one part of the nerve cell to another (the axon
is the long threadlike extension that conducts nerve impulses away
from the body of a nerve cell, and dendrites are
any of the short branched threadlike extensions that conduct nerve
impulses towards the nerve cell body. In Alzheimer's
disease the tau protein is abnormal and the microtubule
structures collapse.
There is an overall shrinkage of brain
tissue as Alzheimer's disease progresses. In addition, the ventricles,
or chambers within the brain that contain cerebrospinal fluid, are
noticeably enlarged. In the early stages of Alzheimer's disease,
short-term memory begins to decline when the cells in the hippocampus,
which is part of the limbic system, degenerate. The ability to
perform routine tasks also declines. As Alzheimer's disease
spreads through the cerebral cortex (the outer
layer of the brain), judgment declines, emotional outbursts may
occur and language is impaired. Progression of the disease leads
to the death of more nerve cells and subsequent behavior changes,
such as wandering and agitation. The ability to recognize faces
and to communicate is completely lost in the final stages.
Patients lose bowel and bladder control, and eventually need
constant care. This stage of complete dependency may last for
years before the patient dies. The average length of time from
diagnosis to death is 4 to 8 years, although it can take 20 years
or more for the disease to run its course.
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Fund established to enhance Alzheimer's disease research
Nancy Humphrey
(graphic by Paul Gross)
Studies of the post-mortem brain tissue of patients afflicted with
Alzheimer¹s Disease will be expanded at Vanderbilt University Medical
Center thanks to money donated in memory of William W. (Bill) Franklin, the
late executive director of Development for VUMC.
FULL STORY
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Comparison
of healthy brain (left) with age-matched brain damaged from Alzheimer's
reveals damage and loss of tissue.
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Alzheimer's Disease (N=46 subjects):
[more information]
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Physician
Home | PET
Clinical Data | PET
Case Studies | Alzheimer's
Disease | Case #3
Alzheimer's Disease - Patient
with memory loss
History
The patient has memory loss. The study was requested to
evaluate for brain metabolism.
PET Findings
Moderate hypometabolism was noted in both posteroparietal
and temporal lobes. The remainder of the scan was
unremarkable.
Other
The hypometabolism noted in the parietal and temporal
lobes is characteristic of Alzheimer's Disease.
Courtesy of
Northern California PET Imaging Center
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History
Patient is a 52-year-old male who has cognitive degeneration. The study was
requested to evaluate brain metabolism.
PET Findings
There is an area of moderate hypometabolism in the left anterior parietal
region. Large areas of moderate to severe hypometabolism are noted in the
posterior parietal region bilaterally that is more prominent on the left.
Moderate hypometabolism is noted in both the temporal lobes. The remainder of
the scan shows no areas of increased or decreased metabolism.
Other
The moderate to severe hypometabolism noted in the temporal and parietal
regions bilaterally is consistent wtih the pattern of Alzheimer's Disease.
Courtesy of
Northern California PET Imaging Center
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I.
Comparison of Healthy and Alzheimer’s Brains
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92 Year Old Male
Cognitively Healthy
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92 Year Old Male
Severe AD
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MRI Movies |
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III. MRI
Viewing Plane
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The Layton Center Neuroimaging Lab utilizes MRI
images from three different planes. These planes are
known as the coronal plane, sagittal plane and
the axial plane. Consequently, we name the
different series of MRI images after the plane in which
they were obtained. Below are images taken from an MRI
series in each plane.
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This page
was last updated on
Thursday, May 5, 2004. Please send your comments to the Layton
Center's Web
Manager.
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Brain Imaging
PET scans are an important part in the diagnosis of cerebral
disorders and also in understanding the causes of brain diseases and
how they can be treated. They can be used in the identification of
movement disorders such as Huntington's and Parkinson's disease, as well as
certain types of epilepsy and psychological disorders e.g. schizophrenia.
Techniques
The images are obtained by tracing the blood flow with water labelled with 15O
or by glucose metabolism with labelled deoxyglucose which has a hydrogen atom
replaced by a 18F atom. The 18F is a better tracer
than 15O since the positron emitted from 18F are of a
lower energy and so it travels a shorter distance before it reacts with an
electron to form two detected photons and so it is more accurate.
However, blood flow gives a better indication of brain function since it is
more sensitive to activity than glucose consumption. In addition, 15O
has a half-life of 2.1 minutes whereas 18F has a half-life of 118
minutes. This means the scan of the blood flow can be repeated up to 12 times
per session so that change in cerebral function can be monitored for different
tasks so that the activity of different areas of the brain can be imaged.
In contrast, deoxyglucose accumulates in the brain over a 30 minute period and
so a task will need to be carried out for this period of time. This
technique is therefore employed for monitoring continuous mental states or the
change caused by a drug if it has a slow effect.
Imaging of Diseases
Epilepsy - Blood flow and glucose uptake are
measured by PET in order to identify seizure sites in the brain. In 80%
of patients there is an increase in blood flow and glucose metabolism during a
seizure in the cerebral cortex. However, between seizure there tends to
be a lower than normal glucose uptake and blood flow.
Parkinson's Disease - Patients have a higher
than normal blood flow to the basal ganglia on the opposite side to the
effected limbs. L-dopa reduces the blood flow to the basal ganglia but
over time can increase the local metabolic rate. There is also a lack of
communication between the frontal and parietal and the frontal occipital
lobes. Glucose metabolism is also decreased generally over the brain by
18% compared to a normal person of a similar age.
Alzheimer's Disease - PET scans show in
patients with mild Alzheimer's and in more advanced cases glucose metabolism
is reduced in both the temporal and parietal lobes. Patients with a
greater amount of language dysfunction than problems with spatial sight
display a significant reduction in metabolism in the left frontal, temporal
and parietal lobes. Cases with greater visual spatial impairment have a
diminished glucose metabolism in the right parietal lobe.
Brain Trauma - Damaged areas of the brain have
a reduced or no blood flow or glucose metabolism. This can be seen in the
images below where there has been a blow to the head by a rock.
►CONTINUE
P.F. Liddle, PET Studies of Cerebral Function in
Schizophrenia in Cambridge Medical Reviews Neurobiology and Psychiatry Vol. 3
Neuroimaging, Ed. R. Kerwin ,Cambridge University Press 1995
H.Holcomb, J, Links, C. Smith, D. Wong, Positron Emission
Tomography: Measuring the Metabolic and Neurochemical Characteristics of the
Living Human Nervous System in Brain Imaging Applications in Psychiatry, Ed.
N. Andreasen, American Psychiatric Press, 1989
http://pet.med.uth.tmc.edu/brain2.html
Brain Functions picture: www.er.doe.gov/feature_articles_2001/June/Decades/92.html
Area of the Brain Diagram: www.sciencebob.com/lab/_bodyzone/brain.html
Epilepsy Pictures: www.biomed.org/pet.html
Brain damage pictures: http://pet.radiology.uiowa.edu/webpage/Research/Casestudies/traumatic_brain_injury.htm
Parkinson's pictures: www.hometown.aol.com/louie2u/_Page2.html
