Tag Archives: Antibody


Immunization, or immunisation, is the process by which an individual’s immune system becomes fortified against an agent (known as the immunogen).It  is the process whereby a person is made immune or resistant to an infectious disease.


Immunization is done through various techniques, most commonly vaccination. Vaccines against microorganisms that cause diseases can prepare the body’s immune system, thus helping to fight or prevent an infection. The fact that mutations can cause cancer cells to produce proteins or other molecules that are known to the body forms the theoretical basis for therapeutic cancer vaccines. Other molecules can be used for immunization as well, for example in experimental vaccines against nicotine (NicVAX) or the hormone ghrelin in experiments to create an obesity vaccine.

Before the introduction of vaccines, the only way people became immune to an infectious disease was by actually getting the disease and surviving it. Smallpox (variola) was prevented in this way by inoculation, which produced a milder effect than the natural disease. It was introduced into England from Turkey by Lady Mary Wortley Montagu in 1721 and used by Zabdiel Boylston in Boston the same year. In 1798 Edward Jenner introduced inoculation with cowpox (smallpox vaccine), a much safer procedure. This procedure, referred to as vaccination, gradually replaced smallpox inoculation, now called variolation to distinguish it from vaccination. Until the 1880s vaccine/vaccination referred only to smallpox, but Louis Pasteur developed immunisation methods for chicken cholera and anthrax in animals and for human rabies, and suggested that the terms vaccine/vaccination should be extended to cover the new procedures. This can cause confusion if care is not taken to specify which vaccine is used e.g. measles vaccine or influenza vaccine.

When this system is exposed to molecules that are foreign to the body, called non-self, it will orchestrate an immune response, and it will also develop the ability to quickly respond to a subsequent encounter because of immunological memory. This is a function of the adaptive immune system. Therefore, by exposing an animal to an immunogen in a controlled way, its body can learn to protect itself: this is called active immunization.

The most important elements of the immune system that are improved by immunization are the T cells, B cells, and the antibodies B cells produce. Memory B cells and memory T cells are responsible for a swift response to a second encounter with a foreign molecule. Passive immunization is direct introduction of these elements into the body, instead of production of these elements by the body itself.

The most important elements of the immune system that are improved by immunization are the T cells, B cells, and the antibodies B cells produce. Memory B cells and memory T cells are responsible for a swift response to a second encounter with a foreign molecule. Passive immunization is direct introduction of these elements into the body, instead of production of these elements by the body itself.

Immunization is a proven tool for controlling and eliminating life-threatening infectious diseases and is estimated to avert between 2 and 3 million deaths each year. It is one of the most cost-effective health investments, with proven strategies that make it accessible to even the most hard-to-reach and vulnerable populations. It has clearly defined target groups; it can be delivered effectively through outreach activities; and vaccination does not require any major lifestyle change.

Immunizations are definitely less risky and an easier way to become immune to a particular disease than risking a milder form of the disease itself. They are important for both adults and children in that they can protect us from the many diseases out there. Through the use of immunizations, some infections and diseases have almost completely been eradicated throughout the United States and the World. One example is polio. Thanks to dedicated health care professionals and the parents of children who vaccinated on schedule, polio has been eliminated in the U.S. since 1979. Polio is still found in other parts of the world so certain people could still be at risk of getting it. This includes those people who have never had the vaccine, those who didn’t receive all doses of the vaccine, or those traveling to areas of the world where polio is still prevalent.

The Immunization can be achieved in an active or passive manner:
Vaccination is an active form of immunization.

Active immunization/vaccination has been named one of the “Ten Great Public Health Achievements in the 20th Century”.

Active immunization:.click & see
Active immunization can occur naturally when a person comes in contact with, for example, a microbe. The immune system will eventually create antibodies and other defenses against the microbe. The next time, the immune response against this microbe can be very efficient; this is the case in many of the childhood infections that a person only contracts once, but then is immune.

Artificial active immunization is where the microbe, or parts of it, are injected into the person before they are able to take it in naturally. If whole microbes are used, they are pre-treated.

The importance of immunization is so great that the American Centers for Disease Control and Prevention has named it one of the “Ten Great Public Health Achievements in the 20th Century”.  Live attenuated vaccines have decreased pathogenicity. Their effectiveness depends on the immune systems ability to replicate and elicits a response similar to natural infection. It is usually effective with a single dose. Examples of live, attenuated vaccines include measles, mumps, rubella, MMR, yellow fever, varicella, rotavirus, and influenza (LAIV).

Passive immunization:……...click & see
Passive immunization is where pre-synthesized elements of the immune system are transferred to a person so that the body does not need to produce these elements itself. Currently, antibodies can be used for passive immunization. This method of immunization begins to work very quickly, but it is short lasting, because the antibodies are naturally broken down, and if there are no B cells to produce more antibodies, they will disappear.

Passive immunization occurs physiologically, when antibodies are transferred from mother to fetus during pregnancy, to protect the fetus before and shortly after birth.

Artificial passive immunization is normally administered by injection and is used if there has been a recent outbreak of a particular disease or as an emergency treatment for toxicity, as in for tetanus. The antibodies can be produced in animals, called “serum therapy,” although there is a high chance of anaphylactic shock because of immunity against animal serum itself. Thus, humanized antibodies produced in vitro by cell culture are used instead if available.



Complications In Pregnancy


Pre-eclampsia, eclampsia or toxemia of pregnancy
Pre-eclampsia or preeclampsia (PE) is a disorder of pregnancy characterized by high blood pressure and a large amount of protein in the urine. The disorder usually occurs in the third trimester of pregnancy and gets worse over time. In severe disease there may be red blood cell breakdown, a low blood platelet count, impaired liver function, kidney dysfunction, swelling, shortness of breath due to fluid in the lungs, or visual disturbances. PE increases the risk of poor outcomes for both the mother and the baby. If left untreated, it may result in seizures at which point it is known as eclampsia.


Toxemia of pregnancy is a severe condition that sometimes occurs in the latter weeks of pregnancy. It is characterized by high blood pressure; swelling of the hands, feet, and face; and an excessive amount of protein in the urine. If the condition is allowed to worsen, the mother may experience convulsions and coma, and the baby may be stillborn.
The term toxemia is actually a misnomer from the days when it was thought that the condition was caused by toxic (poisonous) substances in the blood. The illness is more accurately called preeclampsia before the convulsive stage and eclampsia afterward.

Preeclampsia affects between 2–8% of pregnancies worldwide. Hypertensive disorders of pregnancy are one of the most common causes of death due to pregnancy. They resulted in 29,000 deaths in 2013 – down from 37,000 deaths in 1990. Preeclampsia usually occurs after 32 weeks; however, if it occurs earlier it is associated with worse outcomes. Women who have had PE are at increased risk of heart disease later in life. The word eclampsia is from the Greek term for lightning. The first known description of the condition was by Hippocrates in the 5th century BCE

Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of preeclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in preeclampsia is not great. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.

In general, none of the signs of preeclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several preeclamptic features, the final proof being their regression after delivery.

The symptoms of toxemia of pregnancy (which may lead to death if not treated) are divided into three stages, each progressively more serious:
Mild preeclampsia symptoms include edema (puffiness under the skin due to fluid accumulation in the body tissues, often noted around the ankles), mild elevation of blood pressure, and the presence of small amounts of protein in the urine.

Severe preeclampsia symptoms include extreme edema, extreme elevation of blood pressure, the presence of large amounts of protein in the urine, headache, dizziness, double vision, nausea, vomiting, and severe pain in the right upper portion of the abdomen.
Eclampsia symptoms include convulsions and coma.

Risk Factors:
Known risk factors for preeclampsia include:

*Nulliparity (never given birth)
*Older age, and diabetes mellitus
*Kidney disease
*Chronic hypertension
*Prior history of preeclampsia
*Family history of preeclampsia
*Advanced maternal age (>35 years)
*Antiphospholipid antibody syndrome
*Multiple gestation
*Having donated a kidney.
*Having sub-clinical hypothyroidism or thyroid antibodies

It is also more frequent in a women’s first pregnancy and if she is carrying twins. The underlying mechanism involves abnormal formation of blood vessels in the placenta amongst other factors. Most cases are diagnosed before delivery. Rarely, preeclampsia may begin in the period after delivery. While historically both high blood pressure and protein in the urine were required to make the diagnosis, some definitions also include those with hypertension and any associated organ dysfunction. Blood pressure is defined as high when it is greater than 140 mmHg systolic or 90 mmHg diastolic at two separate times, more than four hours apart in a women after twenty weeks of pregnancy. PE is routinely screened for during prenatal care.
There is no definitive known cause of preeclampsia, though it is likely related to a number of factors. Some of these factors include:

*Abnormal placentation (formation and development of the placenta)
*Immunologic factors
*Prior or existing maternal pathology – preeclampsia is seen more at a higher incidence in individuals with preexisting hypertension, obesity, antiphospholipid antibody syndrome, and those with history of preeclampsia
*Dietary factors, e.g. calcium supplementation in areas where dietary calcium intake is low has been shown to reduce the risk of preeclampsia.
*Environmental factors, e.g. air pollution
*Those with long term high blood pressure have a risk 7 to 8 times higher than those without.

Physiologically, research has linked preeclampsia to the following physiologic changes: alterations in the interaction between the maternal immune response and the placenta, placental injury, endothelial cell injury, altered vascular reactivity, oxidative stress, imbalance among vasoactive substances, decreased intravascular volume, and disseminated intravascular coagulation.

While the exact cause of preeclampsia remains unclear, there is strong evidence that a major cause predisposing a susceptible woman to preeclampsia is an abnormally implanted placenta. This abnormally implanted placenta is thought to result in poor uterine and placental perfusion, yielding a state of hypoxia and increased oxidative stress and the release of anti-angiogenic proteins into the maternal plasma along with inflammatory mediators. A major consequence of this sequence of events is generalized endothelial dysfunction. The abnormal implantation is thought to stem from the maternal immune system’s response to the placenta and refers to evidence suggesting a lack of established immunological tolerance in pregnancy. Endothelial dysfunction results in hypertension and many of the other symptoms and complications associated with preclampsia.

One theory proposes that certain dietary deficiencies may be the cause of some cases. Also, there is the possibility that some forms of preeclampsia and eclampsia are the result of deficiency of blood flow in the uterus.

Pre-eclampsia is diagnosed when a pregnant woman develops:

*Blood pressure >_ 140 mm Hg systolic or  >_  90 mm Hg diastolic on two separate readings taken at least four to six hours apart after 20 weeks gestation in an individual with previously normal blood pressure.
*In a woman with essential hypertension beginning before 20 weeks gestational age, the diagnostic criteria are: an increase in systolic blood pressure (SBP) of   >_ 30mmHg or an increase in diastolic blood pressure (DBP) of   >_15mmHg.
*Proteinuria  >_ 0.3 grams (300 mg) or more of protein in a 24-hour urine sample or a SPOT urinary protein to creatinine ratio  >_ 0.3 or a urine dipstick reading of 1+ or greater (dipstick reading should only be used if other quantitative methods are not available)

Suspicion for preeclampsia should be maintained in any pregnancy complicated by elevated blood pressure, even in the absence of proteinuria. Ten percent of individuals with other signs and symptoms of preeclampsia and 20% of individuals diagnosed with eclampsia show no evidence of proteinuria. In the absence of proteinuria, the presence of new-onset hypertension (elevated blood pressure) and the new onset of one or more of the following is suggestive of the diagnosis of preeclampsia:

*Evidence of kidney dysfunction (oliguria, elevated creatinine levels)
*Impaired liver function (impaired liver function tests)
*Thrombocytopenia (platelet count <100,000/microliter)
*Pulmonary edema
*Ankle edema pitting type
*Cerebral or visual disturbances
*Preeclampsia is a progressive disorder and these signs of organ dysfunction are indicative of severe preeclampsia. A systolic blood pressure ?160 or diastolic blood pressure ?110 and/or proteinuria >5g in a 24-hour period is also indicative of severe preeclampsia. Clinically, individuals with severe preeclampsia may also present epigastric/right upper quadrant abdominal pain, headaches, and vomiting. Severe preeclampsia is a significant risk factor for intrauterine fetal death.

Of note, a rise in baseline blood pressure (BP) of 30 mmHg systolic or 15 mmHg diastolic, while not meeting the absolute criteria of 140/90, is still considered important to note, but is not considered diagnostic.

Predictive tests:
There have been many assessments of tests aimed at predicting preeclampsia, though no single biomarker is likely to be sufficiently predictive of the disorder. Predictive tests that have been assessed include those related to placental perfusion, vascular resistance, kidney dysfunction, endothelial dysfunction, and oxidative stress. Examples of notable tests include:

*Doppler ultrasonography of the uterine arteries to investigate for signs of inadequate placental perfusion. This test has a high negative predictive value among those individuals with a history of prior preeclampsia.
*Elevations in serum uric acid (hyperuricemia) is used by some to “define” preeclampsia,[14] though it has been found to be a poor predictor of the disorder. Elevated levels in the blood (hyperuricemia) are likely due to reduced uric acid clearance secondary to impaired kidney function.
*Angiogenic proteins such as vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) and anti-angiogenic proteins such as soluble fms-like tyrosine kinase-1 (sFlt-1) have shown promise for potential clinical use in diagnosing preeclampsia, though evidence is sufficient to recommend a clinical use for these markers.
*Recent studies have shown that looking for podocytes, specialized cells of the kidney, in the urine has the potential to aid in the prediction of preeclampsia. Studies have demonstrated that finding podocytes in the urine may serve as an early marker of and diagnostic test for preeclampsia. Research is ongoing.

Differential diagnosis:
Pre-eclampsia can mimic and be confused with many other diseases, including chronic hypertension, chronic renal disease, primary seizure disorders, gallbladder and pancreatic disease, immune or thrombotic thrombocytopenic purpura, antiphospholipid syndrome and hemolytic-uremic syndrome. It must be considered a possibility in any pregnant woman beyond 20 weeks of gestation. It is particularly difficult to diagnose when preexisting disease such as hypertension is present. Women with acute fatty liver of pregnancy may also present with elevated blood pressure and protein in the urine, but differs by the extent of liver damage. Other disorders that can cause high blood pressure include thyrotoxicosis, pheochromocytoma, and drug misuse
Preeclampsia and eclampsia cannot be completely cured until the pregnancy is over. Until that time, treatment includes the control of high blood pressure and the intravenous administration of drugs to prevent convulsions. Drugs may also be given to stimulate the production of urine. In some severe cases, early delivery of the baby is needed to ensure the survival of the mother.

Recommendations for prevention include: aspirin in those at high risk, calcium supplementation in areas with low intake, and treatment of prior hypertension with medications. In those with PE delivery of the fetus and placenta is an effective treatment. When delivery becomes recommended depends on how severe the PE and how far along in pregnancy a person is. Blood pressure medication, such as labetalol and methyldopa, may be used to improve the mother’s condition before delivery. Magnesium sulfate may be used to prevent eclampsia in those with severe disease. Bedrest and salt intake have not been found to be useful for either treatment or prevention.

Protein or calorie supplementation have no effect on preeclampsia rates, and dietary protein restriction does not appear to increase preeclampsia rates. Further, there is no evidence that changing salt intake has an effect.

Supplementation with antioxidants such as vitamin C and E has no effect on preeclampsia incidence, nor does supplementation with vitamin D. Therefore, supplementation with vitamins C, E, and D is not recommended for reducing the risk of pre-eclampsia.

Calcium supplementation of at least 1 gram per day is recommended during pregnancy as it prevents preeclampsia where dietary calcium intake is low, especially for those at high risk. Low selenium status is associated with higher incidence of preeclampsia.

Taking aspirin is associated with a 1% to 5% reduction in preeclampsia and a 1% to 5% reduction in premature births in women at high risk. The WHO recommends low-dose aspirin for the prevention of preeclampsia in women at high risk and recommend it be started before 20 weeks of pregnancy. The United States Preventive Services Task Force recommends a low-dose regimen for women at high risk beginning in the 12th week.

Physical activity:
There is insufficient evidence to recommend either exercise or strict bedrest as preventative measures of pre-eclampsia.

Smoking cessation:
In low-risk pregnancies the association between cigarette smoking and a reduced risk of preeclampsia has been consistent and reproducible across epidemiologic studies. High-risk pregnancies (those with pregestational diabetes, chronic hypertension, history of preeclampsia in a previous pregnancy, or multifetal gestation) showed no significant protective effect. The reason for this discrepancy is not definitively known; research supports speculation that the underlying pathology increases the risk of preeclampsia to such a degree that any measurable reduction of risk due to smoking is masked. However, the damaging effects of smoking on overall health and pregnancy outcomes outweighs the benefits in decreasing the incidence of preeclampsia. It is recommended that smoking be stopped prior to, during and after pregnancy

Restriction of salt in the diet may help reduce swelling, it does not prevent the onset of high blood pressure or the appearance of protein in the urine. During prenatal visits, the doctor routinely checks the woman’s weight, blood pressure, and urine. If toxemia is detected early, complications may be reduced.


‘Super Antibody’ Fights Off Flu

The first antibody which can fight all types of the influenza A virus has been discovered, researchers claim.

Experiments on flu-infected mice, published in Science Express, showed the antibody could be used as an “emergency treatment“.

It is hoped the development will lead to a “universal vaccine” – currently a new jab has to be made for each winter as viruses change.

Virologists described the finding as a “good step forward”.

Many research groups around the world are trying to develop a universal vaccine. They need to attack something common to all influenza which does not change or mutate.

It is verymuch suggested that  some people who had swine flu may develop ‘super immunity’ to other infections.

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Source : BBC News,July 29,2011

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Freedom From the Daily JAB

Indian scientists are using tissue engineering to give diabetes patients new insulin-making cells……...CLICK & SEE

Biomaterials scientist Prabha Nair is pitting her expertise of polymers to hold out a new line of hope for patients with diabetes who are dependent on insulin shots. In her laboratory, she has used two structures fashioned out of polymer materials to normalise blood sugar in rats with diabetes for up to 90 days. One of the polymer structures is designed to make insulin-secreting cells function properly, while the other is intended to protect such cells from threats that might emerge from the body’s immune system.

Nair and her colleagues at the government-funded Sree Chitra Tirunal Institute of Medical Sciences and Technology (SCTIMST), Thiruvananthapuram have combined two applications of polymers to tackle two major obstacles that have held back a promising but experimental treatment for diabetes from widespread use. The treatment, called islet cell transplantation, involves the removal of insulin-secreting cells from the pancreas of a deceased organ donor and their implantation into a patient with diabetes.

It is nearly a decade since researchers at the University of Alberta in Edmonton, Canada, demonstrated that islet cell transplantation may help patients with diabetes acquire normal blood sugar levels and achieve some level of freedom from the need for insulin.

A review of islet transplantation on 225 patients between 1999 and 2006 had revealed several benefits — including reduced need for insulin, improved blood glucose control, and lowered risk of hypoglycemia, according to the National Institute of Diabetes and Digestive and Kidney Disorders in the US. Two years after the islet transplantation, about one-third of the recipients were free of the need for insulin shots, the review suggested.

Islet cell transplantation, however, is not standard therapy yet. “There is a critical shortage of islet cells because of a shortage of organ donors,” says Nair, a scientist in the division of tissue engineering and regeneration technologies at the SCTIMST.

Patients who receive islet cells need to take immunosuppressive drugs throughout their lives to prevent their immune systems from destroying the implanted cells. These drugs have side effects including an increased risk of cancer.

The SCTIMST researchers harvested a class of cells known as pancreatic progenitor cells from mice and placed them in a cocktail of appropriate biochemicals where they turn into insulin-secreting islet-like cells.

The scientists then loaded these islet-like cells into three-dimensional scaffolds constructed out of a gelatin, a natural polymer, and polyvinylpyrrolidone, a synthetic polymer. The islet-like cells proliferate on the scaffolds and serve as a potential source of insulin.

In experiments, the scientists observed that rats with diabetes that received these islet cell-bearing scaffolds alone died within 20 days. Their scaffold cells had been attacked by the rats’ immune systems, leading to the destruction of tissue and the failure of the implantation.

“We also designed a polymer capsule to shield the implanted islet cells from the immune system,” Nair told KnowHow. When the scientists combined the scaffolding, also called tissue engineering, with encapsulation, the rats survived for up to 90 days.

The rats were models for type-I, or insulin-dependent diabetes, but researchers say the tissue engineering and encapsulation strategy may also be considered as a possible option for patients with adult-onset diabetes who need insulin injections. Given the differences in the lifespans of rats and humans, some researchers believe the 90-day freedom from insulin observed in the laboratory animals may be equivalent to several years in humans — although exactly how long is still a subject of debate.

“These results are really exciting,” says Aroop Dutta, a tissue engineering specialist and founder of ExCel Matrix Biologicals, a Hyderabad-based start-up in biomaterials and tissue engineering, who was not connected with the research in Thiruvananthapuram.

“There just aren’t enough human-derived islet cells for the large numbers of diabetes patients dependent on insulin. Animal cells or stem cell-based approaches are the only viable options as sustained sources of islet cells,” he adds.

The results of the SCTIMST’s experiments were published last Friday in the journal Acta Biomaterialia. The researchers say their use of islet cells from mice in rats with diabetes suggests that the polymer capsule that keeps the immune system at bay may facilitate xenotransplants — the use of cells or organs across species — as an option for reversing diabetes. “But there is still much work to be done,” Nair cautions.

“We’ll need to establish that this also works in large animals,” she said. The SCTIMST group plans to initiate studies in pigs with diabetes. If the technique is indeed shown to work in large animals too, it could be ready for human clinical trials within two or three years.

Source : The Telegraph ( kolkata, India)

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Foe Turns Friend

A-beta, a protein implicated in Alzheimer’s, may be the brain’s shield against germs.
For years, a prevailing theory has been that one of the chief villains in Alzheimer’s disease has no real function other than as a waste product that the brain never properly disposed of.

The material, a protein called beta amyloid, or A-beta, piles up into tough plaques that destroy signals between nerves. When that happens, people lose their memory, their personality changes and they stop recognising friends and family.

But now researchers at Harvard suggest that the protein has a real and unexpected function — it may be part of the brain’s normal defences against invading bacteria and other microbes.

Other Alzheimer’s researchers say the findings, reported in the current issue of the journal PLoS One, are intriguing.

The new hypothesis got its start late one Friday evening in the summer of 2007 in a laboratory at Harvard Medical School. The lead researcher, Rudolph Tanzi, a neurology professor who is also director of the genetics and aging unit at Massachusetts General Hospital, said he had been looking at a list of genes that seemed to be associated with Alzheimer’s disease.

To his surprise, many looked just like genes associated with the so-called innate immune system, a set of proteins the body uses to fight infections. The system is particularly important in the brain, because antibodies cannot get through the blood-brain barrier, the membrane that protects the brain. When the brain is infected, it relies on the innate immune system to protect it.

That evening, Tanzi wandered into the office of a junior faculty member, Robert Moir, and mentioned what he had seen. As Tanzi recalled, Moir turned to him and said, “Yeah, well, look at this.”

He handed Tanzi a spreadsheet. It was a comparison of A-beta and a well-known protein of the innate immune system, LL-37. The likenesses were uncanny. Among other things, the two proteins had similar structures. And like A-beta, LL-37 tends to clump into hard little balls.

In rodents, the protein that corresponds to LL-37 protects against brain infections. People who make low levels of LL-37 are at increased risk of serious infections and have higher levels of atherosclerotic plaques, arterial growths that impede blood flow.

The scientists could hardly wait to see if A-beta, like LL-37, killed microbes. They mixed A-beta with microbes that LL-37 is known to kill — listeria, staphylococcus, pseudomonas. It killed eight out of 12. “We did the assays exactly as they have been done for years,” Tanzi said. “And A-beta was as potent or, in some cases, more potent than LL-37.”

Then the investigators exposed the yeast Candida albicans, a major cause of meningitis, to tissue from the hippocampal regions of brains from people who had died of Alzheimer’s and from people of the same age who did not have dementia when they died.

Brain samples from Alzheimer’s patients were 24 per cent more active in killing the bacteria. But if the samples were first treated with an antibody that blocked A-beta, they were no better than brain tissue from non-demented people in killing the yeast.

The innate immune system is also set in motion by traumatic brain injuries and strokes and by atherosclerosis that causes reduced blood flow to the brain, Tanzi noted.

And the system is spurred by inflammation. It’s known that patients with Alzheimer’s have inflamed brains, but it hasn’t been clear whether A-beta accumulation was a cause or an effect of the inflammation. Perhaps, Tanzi said, A-beta levels rise as a result of the innate immune system’s response to inflammation; it may be a way the brain responds to a perceived infection. But does that mean Alzheimer’s disease is caused by an overly exuberant brain response to an infection?

That’s one possible reason, along with responses to injuries and inflammation and the effects of genes that cause A-beta levels to be higher than normal, Tanzi said. However, some researchers say that all the pieces of the A-beta innate immune systems hypothesis are not in place.

Dr Norman Relkin, director of the memory disorders programme at New York-Presbyterian / Weill Cornell hospital, said that although the idea was “unquestionably fascinating”, the evidence for it was “a bit tenuous”.

As for the link with infections, Dr Steven DeKosky, an Alzheimer’s researcher at the Virginia School of Medicine, noted that scientists have long looked for evidence linking infections to Alzheimer’s and have come up mostly empty handed.

But if Tanzi is correct about A-beta being part of the innate immune system, that would raise questions about the search for treatments to eliminate the protein from the brain.

“It means you don’t want to hit A-beta with a sledgehammer,” Tanzi said.

But other scientists not connected with the discovery said they were impressed by the new findings. “It changes our thinking about Alzheimer’s disease,” said Dr Eliezer Masliah, who heads the experimental neuropathology laboratory at the University of California, San Diego.

Source : New York Times News Service

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