Gram stain: negative Cell shape: bacillus Arrangement: Oxygen requirements: facultative anaerobe Motility: motile Other: Produces red pigment at room temperature.
Habitat: Occurs naturally in soil and water as well as the intestines.
Pathogenicity: Important as a nocosomial infection; associated with urinary and respiratory tract infections, endocarditis, osteomyelitis, septicemia, wound infections, eye infections, meningitis.
Transmission: direct contact, droplets; has been found growing on catheters, in saline irrigation solutions, and in other supposedly sterile solutions.
Treatment: Includes cephalosporins, gentamicin, amikacin, but most strains are resistant to several antibiotics because of the presence or R-factors on plasmids.
We used to think that this bacteria was non-pathogenic, and because of the pigment it produces, it was used widely to trace bacterial transmission. In 1951 and 1952 the US Army conducted a study called "Operation Sea-Spray" to study wind currents that might carry biological weapons. They filled balloons with S. marcescens and burst them over San Francisco. Shortly thereafter, doctors noted a drastic increase in pneumonia and urinary tract infections.
Serratia marcescens is a Gram negative, bacillus shaped bacteria that belongs to the family Enterobacteriaceae. In 1819, Bartolomeo Bizio, an Italian pharmacist from Padua, discovered S. marcescens. Bizio identified the bacterium as the cause of the miraculous bloody discoloration of cornmeal mush, or polenta. He named Serratia in honor of the Italian physicist Serratia who invented the steamboat, and named marcescens from the Latin word for decaying because the bloody coloration quickly disappeared. Key characteristics of S. marcescens include the production of Dnase, lipase and gelatinase, and it is oxidase negative. These bacteria grow well on standard media and produce a red to dark pink pigment that aids in identification. 1
Alzheimer's treatments currently work by temporarily improving symptoms of memory loss and problems with thinking and reasoning. These Alzheimer's treatments boost performance of specialized biochemicals that carry information from one brain cell to another. But they don't stop the underlying decline and death of brain cells. As more cells die, Alzheimer's continues to progress.
Alzheimer's disease is characterised by loss of neurons and synapses in the cerebral cortex and certain subcortical regions. This loss results in gross atrophy of the affected regions, including degeneration in the temporal lobe and parietal lobe, and parts of the frontal cortex and cingulate gyrus.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid12934968-33|]] Studies using MRI and PET have documented reductions in the size of specific brain regions in patients as they progressed from mild cognitive impairment to Alzheimer's disease, and in comparison with similar images from healthy older adults.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-54|]]
Both amyloid plaques and neurofibrillary tangles are clearly visible by microscopy in brains of those afflicted by AD.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid15184601-10|]] Plaques are dense, mostly insoluble deposits of amyloid-beta peptide and cellular material outside and around neurons. Tangles (neurofibrillary tangles) are aggregates of the microtubule-associated protein tau which has become hyperphosphorylated and accumulate inside the cells themselves. Although many older individuals develop some plaques and tangles as a consequence of aging, the brains of AD patients have a greater number of them in specific brain regions such as the temporal lobe.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid8038565-55|]] Lewy bodies are not rare in AD patient's brains.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid11816795-56|]]
Enzymes act on the APP (amyloid precursor protein) and cut it into fragments. The beta-amyloid fragment is crucial in the formation of senile plaques in AD.Alzheimer's disease has been identified as a protein misfolding disease (proteopathy), caused by accumulation of abnormally folded A-beta and tau proteins in the brain.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid14528050-57|]] Plaques are made up of small peptides, 39–43 amino acids in length, called beta-amyloid (also written as A-beta or Aβ). Beta-amyloid is a fragment from a larger protein called amyloid precursor protein (APP), a transmembrane protein that penetrates through the neuron's membrane. APP is critical to neuron growth, survival and post-injury repair.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid16822978-58|]][[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid12927332-59|]] In Alzheimer's disease, an unknown process causes APP to be divided into smaller fragments by enzymes through proteolysis.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid15787600-60|]] One of these fragments gives rise to fibrils of beta-amyloid, which form clumps that deposit outside neurons in dense formations known as senile plaques.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid15184601-10|]][[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid15004691-61|]]
http://en.wikipedia.org/wiki/File:TANGLES_HIGH.jpg In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells.AD is also considered a tauopathy due to abnormal aggregation of the tau protein. Every neuron has a cytoskeleton, an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell to the ends of the axon and back. A protein called tau stabilizes the microtubules when phosphorylated, and is therefore called a microtubule-associated protein. In AD, tau undergoes chemical changes, becoming hyperphosphorylated; it then begins to pair with other threads, creating neurofibrillary tangles and disintegrating the neuron's transport system.[[http://en.wikipedia.org/wiki/Alzheimer's#cite_note-pmid17604998-62|]]
Comparison of a normal aged brain (left) and an Alzheimer's patient's brain (right). http://en.wikipedia.org/wiki/Alzheimer%27s
The section below has a lot of useful information and can help guide your research with good questions you should be able to answer.
These people invented the robot, but what will you do WITH this robot?...
At the NanoRobotics Lab at Carnegie Melon University (Pittsburgh, PA) they have designed a truly microscale swimming robot. (characteristic length of the robot doesn't exceed 100 μm, the size of a small bacteria)
“Bacteria are attached to Polystyrene (PS) microspheres via electrostatic, van der waals and hydrophobic interactions. As the attached bacteria rotate their flagella they push the microsphere forward. The on/off motion of the microspheres is controlled by introducing different chemicals into the experimental environment. To stop the motion, copper ions are introduced. These ions bond to the rotor of the flagellar motor and prevent its motion. To resume the motion we introduce another chemical called ethylenediaminetetraacetic acid (EDTA), which traps the copper ions attached to the rotor of the flagellar motor, allowing it to resume its motion.
Benefits: We envision this robot having the capability to swim to inaccessible areas in human body and perform complicated user directed tasks such as diagnosis of diseases at early stages and targeted drug delivery.”
What are electrostatic, van der waals and hydrophobic interactions? These are forces that control protein structure…creating a 3D structure.
Team 1: Send gene therapy to the brain to reverse or stop Alzheimer's.
Team 2: Send drugs (monoclonal antibodies) to the brain to treat brain tumors.
Main Problem: How will you get your medicine into the brain with this robot? Overcoming the difficulty of delivering therapeutic agents to specific regions of the brain presents a major challenge to treatment of most brain disorders.
Your solution: microscale swimming robot
What is blood-brain barrier?
The blood-brain barrier acts very effectively to protect the brain from many common bacterial infections. Viruses and a few bacteria (that cause meningitis) easily bypass the blood-brain barrier by attaching themselves to circulating immune cells.
The blood-brain barrier keeps out potentially beneficial drugs. Only 2% of small-molecule compounds enter the brain on their own, even though they cross easily into other tissues.
(Molecules are considered small if they're less than 400 daltons, roughly the size of sucrose.) No large molecules cross—no monoclonal antibodies, no gene therapies, no antisense and RNA interference compounds, no recombinant proteins. “We have come up with a number of potential agents that could benefit humans,” says Thomas Jacobs, a program officer at the US National Institute for Neurological Disorders and Stroke (NINDS) who directs both stroke and blood-brain barrier research, “but we run into a major roadblock when we try to deliver them to the nervous system.”
Endothelial cells restrict the diffusion of microscopic objects (e.g. bacteria) and large or hydrophilic molecules into the CSF, while allowing the diffusion of small hydrophobic molecules (O2, hormones, CO2). Cells of the barrier actively transport metabolic products such as glucose across the barrier with specific proteins.
However, some bacteria do cross the barrier…but how? Remember you are using a modified bacteria…so this could be your key…
The target receptor for bacteria causing meningitis (a bacterial infection of the brain) (Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenza) is on the receptor for the structural protein laminin (serving as the scaffold for blood vessel walls).
® When bacteria adhere to the laminin receptor, the event triggers a biochemical cascade, opening the door into blood vessel cells. Those endothelial cells provide their route into the brain.
So, now you have an idea of how to get your micro robot into the brain.
What will your robot take into the brain?
'Two ideas: Gene Therapy or Monoclonal Antibodies
What is a gene? a segment of DNA that is involved in producing a polypeptide chain. It carries blueprints — the instructions — for making proteins. Proteins are the building blocks for everything in your body. Bones and teeth, hair and earlobes, muscles and blood, all are made up of proteins (as well as other stuff).
What is gene therapy? Any of several therapies involving the insertion of genes into a patient's cells in order to replace defective ones. What is a virus? a piece of nucleic acid (DNA or RNA) wrapped in a thin coat of protein that can replicate only inside the cells of other organisms. So is it alive?
What is nucleic acid? The most common nucleic acids are deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). ...which form nucleotide chains that are vital constituents of all living cells. They carry the genetic information to make an organism, which is passed between generations.
What is AAV? Adeno-associated viruses, are small viruses with a genome of single stranded DNA. The recombinant (definition ?) AAV, which does not contain any viral genes and only the therapeutic gene
How do the researchers control the flagella attached to the microbead? (see original statement at top of page)
Why is your idea (micro swimming robot) a good one?
What images can you create for the display board?
What is Alzheimer's? A disease that is the most common cause of dementia characterized by progressive neurodegeneration.
What is dementia?
Dementia is the term used to describe the symptoms of a large group of illnesses which cause a progressive decline in a person's mental functioning. It is a broad term which describes a loss of memory, intellect, rationality, social skills and normal emotional reactions.
Can gene therapy reverse Alzheimer's?
Sept. 21, 2005 - In mice, that had been genetically engineered to develop Alzheimer's disease, scientists were able to dramatically reverse the rodents' severe memory loss by reducing the amount of an enzyme that is crucial for the development of Alzheimer's disease. (http://seniorjournal.com/NEWS/Alzheimers/5-09-21AlzheimersReversed.htm)
In the past, gene therapy has been mainly used to deliver normal genes into cells to compensate for defective versions of the gene causing disease. In their study, the researchers used gene therapy to silence a normally functioning gene. Exploiting a mechanism called RNA interference, they were able to turn down the gene that helps produce the characteristic amyloid plaques that are one of the hallmarks of Alzheimer's disease.
"Within a month of treatment, mice that had already suffered memory deficits could learn and remember how to find their way through a water maze," says co-author Robert Marr, a post-doctoral researcher in Verma's lab.
A modified lentivirus, which has been developed in Verma's lab, delivered the siRNAs (small pieces of genetic material) into the brain cells (micro robot for this use?) of the transgenic mice that were producing vast amounts of human beta-amyloid and whose brains where littered with plaques.
What are transgenic mice?
What is human beta-amyloid?
What are plaques?
What kind of brain tumors are there? One example:
® Glial cells, the most common cells in the brain, make up the brain's supportive tissue and are the main source of central nervous system tumors. Tumors that arise from these cells are called gliomas. The most common kind of glioma is called an astrocytoma because it arises from a kind of glial cell called an astrocyte. Half of all primary brain tumors are glial cell tumors, and three quarters of gliomas are astrocytomas.
Is this a difficult tumor to treat?
How do they treat brain tumors?
Treatment for anaplastic astrocytoma includes immunotherapy, gene therapy, biological therapy, radiation, surgery, chemotherapy, and hormone therapy.
One possible treatment involves monoclonal antibodies that bind only to cancer cell-specific antigens and induce an immunological response against the target cancer cell.
What does this mean? So antibodies attack foreign invaders in our blood (usually viruses, etc). If we create specific ones in the lab that recognize the cancer, they will help the body attack the cancer cell.
A new study published today in Clinical Cancer Research found that treatment with a novel monoclonal antibody (definition?) (mAb) L2G7 inhibited the growth of glioma cells, induced glioma regression within the brain and prolonged survival. (http://www.medicalnewstoday.com/articles/37887.php )
What is a monoclonal antibody? (http://en.wikipedia.org/wiki/Monoclonal_antibodies)
Antibodies (also known as immunoglobulins) are gamma globulin proteins that are found in blood or other bodily fluids of vertebrates, and are used by the immune system to identify and neutralize foreign objects, such as bacteria and viruses.
So a monoclonal antibody is any of the highly specific antibodies produced in large quantity by the clones of a single' hybrid by the fusion of a B cell with a tumor cell. cell formed in the laboratory
A monoclonal antibody is a laboratory-produced molecule that's carefully engineered to attach to specific defects in cancer cells. Monoclonal antibodies mimic the antibodies your body naturally produces as part of your immune system's response to germs, vaccines and other invaders.
Monoclonal antibodies are administered through a vein (intravenously). Some monoclonal antibody drugs may be used in combination with other treatments, such as chemotherapy. Others are administered alone.
Can you attach this to your robot?
From above: “One possible treatment involves monoclonal antibodies that bind only to cancer cell-specific antigens and induce an immunological response against the target cancer cell”. What is an immunological response? Why will this kill the tumor cells?
According to the World Health Organization (WHO) there are four grades of brain tumors that are derived from astrocytes which are a type of neuroglial brain cell. These tumors are called astrocytomas. These various types of astrocytomas include:
High grade astrocytomas such as Anaplastic astrocytoma and Glioblastoma multiforme infiltrate surrounding brain tissue and, therefore, complete surgical removal is usually not possible. These cancers are usually fatal although prolonged survival does occur in a small minority of patients.
Radiation after surgery prolongs survival for a few months. The roles of sterotaxic radiosurgery and interstital brachytherapy are uncertain. Sterotaxic radiosurgery is the administration of a highly focused dose of radiation. Examples of this include gamma knife. Interstital brachytherapy is the placement of radioactive material directly into the tumor. This approach is associated with necrosis (i.e. death) of normal brain tissue.
Chemotherapy is only marginally effective in the treatment of Anaplastic astrocytoma and Glioblastoma multiforme. Typical chemotherapy agents include carmustine (BCNU) and lomustine (CCNU).
Today, there are some encouraging published results with immunotherapy and biologic therapies (i.e. radio-immunotherapy, retinoid therapy, and vitamin analogs). The Cancer Monthly database currently has the results (survival, side effects, etc.) for 100 recent therapies for glioblastoma multiforme and 22 recent therapies for anaplastic astrocytoma including: immunotherapy, gene therapy, biological therapy, radiation, surgery, chemotherapy, and hormone therapy.
Gliomas and Astrocytomas
Glial cells, the most common cells in the brain, make up the brain's supportive tissue and are the main source of central nervous system tumors. Tumors that arise from these cells are called gliomas. The most common kind of glioma is called an astrocytoma because it arises from a kind of glial cell called an astrocyte. Half of all primary brain tumors are glial cell tumors, and three quarters of gliomas are astrocytomas.
The initial symptoms of brain tumors, such as headache and nausea, usually are the result of increased intracranial pressure caused by the bulk of the tumor or a backup of the cerebrospinal fluid that surrounds the brain and spinal cord. The glial cells are widely distributed throughout the central nervous system, so these tumors can occur in a wide variety of locations, and therefore can cause a wide variety of other symptoms. Depending on the location of the mass, gliomas may cause seizures, weakness or numbness in the limbs, impairments in language function, blurred or double vision, gradual changes in mood or personality, and memory loss.
Imaging studies are the key component in the diagnosis of gliomas. Currently, magnetic resonance imaging (MRI) is the best available imaging modality. Computed tomography (CT) scans also are used. For either study, an agent that provides contrast in the image is administered intravenously so neurological surgeons can visualize the tumor against the normal brain in the background. In some cases, neurological surgeons may employ an MRI scan with frameless stereotactic guidance. For this study, a contrast MRI is performed after special markers (called fiducials) are placed on the patient's scalp. The fiducials are processed by a computer, which calculates the location of the tumor and creates a three-dimensional reconstruction. This image then is used at the time of surgery to help locate the tumor precisely, maximize tumor removal, and minimize injury to the surrounding brain.
Surgery for gliomas involves the resection of the tumor to decrease the pressure it exerts. For most gliomas, however, surgery will not provide a cure by itself. When a tumor is removed, it can be examined under a microscope to provide an accurate diagnosis so the next steps in treatment, which may include radiation therapy or chemotherapy, can be determined. In addition, some smaller tumors may be treated effectively with stereotactic radiosurgery, which involves the use of a highly focused beam of radiation to target the cancer cells specifically and leave the surrounding brain unaffected. The choice of treatment usually is made based on the grade of the tumor, which is a measure of the tumor's malignancy.
New Targeted Brain Tumor Treatment Shows Promise In Pre-clinical Models
Gliomas are the most common primary brain tumors, and also one of the most complicated cancers to treat. Currently, treatment options such as surgery, radiation and chemotherapy are only marginally beneficial and present significant risks for patients, including loss of physical and cognitive abilities.
But, a new study published today in Clinical Cancer Research found that treatment with a novel monoclonal antibody (definition?) (mAb) L2G7 inhibited the growth of glioma cells, induced glioma regression within the brain and prolonged survival - a finding that could be translated into human trials as early as next year.
"There is a tremendous need for advancement in the treatment of malignant brain tumors, which are the number one cancer killer of children under age 20 and a devastating diagnosis for adults as well," said Dr. John Laterra, M.D., Ph.D., research scientist at the Kennedy Krieger Institute and senior author of the study. "The results of this study bring us closer to developing an alternative treatment option for both adults and for pediatric patients, who are hardest hit by conventional therapies."
A team of researchers, led by Dr. Jin Kim of Galaxy Biotech, LLC in Mountain View, CA and Dr. John Laterra of the Kennedy Krieger Institute in Baltimore, MD, designed the study to evaluate the effectiveness of L2G7 in treating human gliomas implanted in mouse models. Results indicate that treatment with L2G7 completely inhibited the growth of the tumors when established under the skin of animals, while control mAb had only a minimal effect.
Even more promising results were observed in mice with tumors implanted within the brain. In this setting, L2G7 not only induced tumor regression, but dramatically increased survival. Animals treated with the control all died within 41 days of starting the experiment. All mice treated with L2G7 survived through day 70, and 80% of the animals were alive at day 90, six weeks after stopping the L2G7 treatment. L2G7 was developed by Dr. Kim's team to inhibit the activities of hepatocyte growth factor (HGF). HGF is known to be a promising target for cancer therapy by virtue of its multiple actions that promote cancer malignancy. HGF stimulates tumor cell division, tumor angiogenesis (blood vessel formation) and tumor cell resistance to toxic agents such as chemotherapy and radiation. In this study, brain tumor cells were injected both under the skin and within the brain to specifically evaluate anti-tumor responses within the central nervous system. The central nervous system is a location often protected from cancer therapies by the "blood-brain barrier," which could possibly limit the effects of mAb therapy on tumors situated within the brain. Treatment with L2G7 or a control mAb was given to both subsets of mice twice weekly. In one experiment, the researchers delayed treatment of a subset of mice for 18 days to determine the effect of L2G7 on larger, more advanced tumors within the brain. At that time, the average tumor size was 26.7 mm3, but following only three doses of L2G7, tumors shrank to 11.7 mm3. Conversely, tumors treated with the control mAb grew 5-fold to 134.3 mm3 during the same period, with a mean volume 12 times larger than the L2G7-treated tumors.
"Monoclonal antibodies to growth factors or their receptors are playing an increasingly important role in cancer therapy," said Dr. Cary Queen, President of Galaxy Biotech. "Because of its specificity for HGF, L2G7 may prove to be particularly effective at halting tumor growth while minimizing side effects and harm to the surrounding healthy brain cells."
There are different types of treatment for patients with adult brain tumors.
Different types of treatment are available for patients with adult brain tumors. Some treatments are standard (the currently used treatment), and some are being tested in clinical trials. A treatment clinical trial is a research study meant to help improve current treatments or obtain information on new treatments for patients with cancer. When clinical trials show that a new treatment is better than the standard treatment, the new treatment may become the standard treatment. Patients may want to think about taking part in a clinical trial. Some clinical trials are open only to patients who have not started treatment.
Three types of standard treatment are used:
Even if the doctor removes all the cancer that can be seen at the time of the surgery, some patients may be given chemotherapy or radiation therapy after surgery to kill any cancer cells that are left. Treatment given after the surgery, to lower the risk that the cancer will come back, is called adjuvant therapy.
Radiation therapy is a cancer treatment that uses high-energy x-rays or other types of radiation to kill cancer cells or keep them from growing. There are two types of radiation therapy. External radiation therapy uses a machine outside the body to send radiation toward the cancer. One type of external radiation therapy is hyperfractionated radiation therapy, in which the total dose of radiation is divided into small doses given more than once a day. Internal radiation therapy uses a radioactive substance sealed in needles, seeds, wires, or catheters that are placed directly into or near the cancer. The way the radiation therapy is given depends on the type of tumor and where it is in the brain.
Chemotherapy is a cancer treatment that uses drugs to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. When chemotherapy is taken by mouth or injected into a vein or muscle, the drugs enter the bloodstream and can reach cancer cells throughout the body (systemic chemotherapy). When chemotherapy is placed directly into the cerebrospinal fluid, an organ, or a body cavity such as the abdomen, the drugs mainly affect cancer cells in those areas (regional chemotherapy). Combination chemotherapy is treatment using more than one anticancer drug. To treat brain tumors, a dissolving wafer may be used to deliver an anticancer drug directly to the brain tumor site after the tumor has been removed by surgery. The way the chemotherapy is given depends on the type of tumor and where it is in the brain.
Gene therapy is the insertion of genes into an individual's cell and biological tissues to treat disease, such as cancer where deleterious mutant alleles are replaced with functional ones. Although the technology is still in its infancy, it has been used with some success. Scientific breakthroughs continue to move gene therapy toward mainstream medicine.
Today, most gene therapy studies are aimed at cancer and hereditary diseases linked to a genetic defect.
Adeno-associated viruses, from the parvovirus family, are small viruses with a genome of single stranded DNA. The recombinant (definition ?) AAV, which does not contain any viral genes and only the therapeutic gene
This type of virus is being used, however, because it is non-pathogenic (most people carry this harmless virus). Most people treated with AAV will not build an immune response to remove the virus and the cells that have been successfully treated with it.
Several trials with AAV are on-going or in preparation, mainly trying to treat muscle and eye diseases; the two tissues where the virus seems particularly useful. However, clinical trials have also been initiated where AAV vectors are used to deliver genes to the brain. This is possible because AAV viruses can infect non-dividing (quiescent) cells, such as neurons in which their genomes are expressed for a long time.
Gene therapy is the treatment of human disease by gene transfer. Many, or maybe most, diseases have a genetic component — asthma, cancer, Alzheimer's disease, for example.
However, most diseases are polygenic, i.e. a subtle interplay of many genes determines the likelihood of developing a disease condition, whereas, so far, gene therapy can only be contemplated for monogenic diseases, in which there is a single gene defect. Even in these cases only treatment of recessive diseases can be considered, where the correct gene is added in the continued presence of the faulty one. Dominant mutations cannot be approached in this way, as it would be necessary to knock out the existing faulty genes in the cells where they are expressed (i.e. where their presence shows an effect), as well as adding the correct genetic information. Gene therapy for recessive monogenic diseases involves introducing correct genetic material into the patient. This can be approached in two different ways. Cells can be taken from the patient, modified in the laboratory (‘in vitro’), and then re-introduced, or a carrier (‘vector’) of the correct genetic material can be delivered directly into the patient. Examples are adenosine deaminase (ADA) deficiency and cystic fibrosis, respectively.
What is alzheimer’s?
Alzheimer's disease is the most common cause of dementia characterized by progressive neurodegeneration.
Dementia is the term used to describe the symptoms of a large group of illnesses which cause a progressive decline in a person's mental functioning. It is a broad term which describes a loss of memory, intellect, rationality, social skills and normal emotional reactions.
Alzheimer's disease is the most common form of dementia and accounts for between 50% and 70% of all cases. It is a progressive, degenerative disease that attacks the brain. In its early phases, the symptoms can be subtle such as memory loss and vagueness, taking longer to do routine tasks, or losing the point of a conversation. As the disease progresses, the changes will become more dramatic until, in the last stages, the person cannot care for themselves. (http://esvc000861.wic015u.server-web.com/faq2.htm)
What Is the Role of Genetics in Familial Alzheimer's Disease?
Alzheimer's disease strikes early and fairly often in certain families, often enough to be singled out as a separate form of the disease and given a label: early-onset familial Alzheimer's disease, or FAD. Combing through the DNA of these families, researchers have found an abnormality in one gene on chromosome 21 that is common to a few of the families. And they have linked a much larger proportion of early-onset families to recently identified and related genes on chromosomes 1 and 14.
The chromosome 21 gene also intrigues Alzheimer's researchers because of its role in Down syndrome. People with Down syndrome have an extra copy of chromosome 21 and, as they grow older, usually develop abnormalities in the brain like those found in Alzheimer's disease.
Doctors are calling for a clinical trial of an experimental drug treatment that it is claimed can reverse the symptoms of Alzheimer's disease "in minutes".
U.S. researchers say the treatment allowed an 82-year- old sufferer to recognise his wife for the first time in years.
In the UK, specialists believe the claims should be properly tested as only a few patients have been treated so far.
A team led by St. Jude investigators has identified the cell surface receptor that bacteria and other infectious agents must dupe to launch their assault on the brain, a finding that raises hope for a new generation of meningitis vaccines.
Writing in the June 1 edition of the Journal of Clinical Investigation, the researchers outlined evidence that the three bacteria responsible for nearly all bacterial meningitis start their journey across the blood-brain barrier at the same receptor. The receptor is on a protein serving as the scaffold for blood vessel walls.
The target receptor for Streptococcus pneumoniae, Neisseria meningitidis and Haemophilus influenzae is on the receptor for the structural protein laminin. Although the three bacteria use different proteins to bind to the laminin receptor (LR), researchers demonstrated the results are the same.
When bacteria adhere to the LR, the event triggers a biochemical cascade, opening the door into blood vessel cells. Those endothelial cells provide their route into the brain. Earlier research found other infectious agents, including viruses, prions and bacterial toxins, use the same LR to gain such access.
Researchers cautioned that other factors are likely involved in helping bacteria across the blood-brain barrier. But evidence of a common receptor raises scientists’ hopes for developing one vaccine against the leading causes of bacterial meningitis. Since viruses and other infectious agents use the same receptor, it might also prove useful for efforts to protect against an even broader array of threats.
For the Display Board:
What is the medical issue (body part) you are trying to treat/cure? Ie. How can modern medicine….how can doctors….treat Alzheimer’s …..cure cancer….here is some current research…brain tumors hard to treat….Alzheimer’s located in the brain…difficult to treat….etc.
Researchers are developing micro robot…at Carnegie….Could this be used to…..?
Describe the parts of the brain (image?). What does it do?
What is Alzheimer’s? How does this affect brain function? Is there a current treatment?
What is a brain tumor?, what types are there?, which tumor would you try to treat? Why? What is the current treatment?
Why is treating the brain so difficult?
Explain the micro swimming robot (image?) What is a flagella? Etc.
Fifth and sixth paragraph:
Explain gene therapy (image?) and examples from research to treat Alzheimers.
How does the robot enhance the gene therapy? How does your idea work? Why will this be a good idea for treating Alzheimer’s?
Explain monoclonal antibodies (image?) and how it would treat brain tumors.
How does the robot work in this treatment? Why will this be a good idea for treating brain tumors?
Identify a scientist working on this problem and tell about him/her. So select robot scientist..or gene therapy scientist, etc.
Report on your team’s interview with doctor/scientist…(to be decided)
Paragraph 1: Our project is about treating Alzheimer’s disease in the brain, using a micro swimming robot. The micro swimming robot brings gene therapy to the affected areas in the brain. Recently, some researchers at the NanoRobotics Lab at Carnegie Melon University in Pittsburgh, PA, have designed a micro scale swimming robot, the size of a small bacteria. Since it is very difficult to bring any drugs into the brain, because of the blood-brain barrier, the micro swimming robot will have to attach itself to the endothelial cells to travel through the blood vessels. That way, the robot will be able to bring gene therapy directly to the brain. Why use gene therapy? On September 21, 2005, scientists made mice develop Alzheimer’s disease. Then, they decreased the amount of a certain enzyme that is needed for the Alzheimer’s disease to develop. This reversed much of the mice’s memory loss. So, we think we could use gene therapy like this in humans, and possibly find a good way to cure Alzheimer’s disease.
paragraph 4: a micro swimming robot that is a small robot that swims through your body to places we can't reach. this robot can perform delivery tasks such as drug delivery tasks such as drug delivery. It swims using its flagellum. flagellum is a tail-like projection that protrudes from the cell body of a certain bacteria functions in locomotion. the flagellum moves the micro swimming robot.
The brain is the most important organ in the body. It has to be protected at all costs. This is why most problems that occur in the brain, are fatal. Alzheimer’s is a fatal problem in the brain. It destroys brain cells that carry information. This means that having Alzheimer’s will make you forget more. Alzheimer’s affects mainly old people because the BBB (blood brain barrier) has been weakened over the 75+ years it has been defending the brain. The BBB keeps all big substances out. Still there are things that get the free pass to the brain because they are covered in fat from the cells that check for bad substances. Alcohol nicotine and caffeine all have the free pass in.
The only other way into the brain is to attach to bigger cells that already have the free pass. This is how Alzheimer’s gets to the brain. The dormant cell is undetected when entering the brain, and then releases mayhem. No cells check the cerebrospinal fluid in the brain because the BBB should have already done that. Alzheimer’s just floats around and kills brain cells, as easy as shooting fish in a barrel. So then medicine comes in, but how does it get by the BBB? It mimics Alzheimer’s disease and enters the brain contained in the micro swimming robot to battle the disease. This is how our micro swimming robot fights Alzheimer’s.