Antibodies are produced in a process of evolution that is still a subject of scientific research. Briefly, antibodies are produced by B cells in two ways: (i) randomly, and (ii) in response to a foreign protein or substance within the body. Initially, one B cell produces one specific kind of antibody. In either case, the B cell is allowed to proliferate or is killed off through a process called clonal deletion. Normally, the immune system is able to recognize and ignore the body’s own healthy proteins, cells, and tissues, and to not overreact to non-threatening substances in the environment, such as foods. Sometimes, however, the immune system ceases to recognize one or more of the body’s normal constituents as “self,” leading to production of pathological autoantibodies. These autoantibodies attack the body’s own healthy cells, tissues, and/or organs, causing inflammation and damage. It should be noted that autoantibodies may also play a nonpathological role; for instance they may help the body to destroy cancers and to eliminate waste products. The role of autoantibodies in normal immune function is also a subject of scientific research.
The causes of autoantibody production are varied and not well understood. It is thought that some autoantibody production is due to a genetic predisposition combined with an environmental trigger, such as a viral illness or a prolonged exposure to certain toxic chemicals. There is generally not a direct genetic link however. While families may be susceptible to autoimmune conditions, individual family members may have different autoimmune disorders, or may never develop an autoimmune condition. Researchers believe that there may also be a hormonal component as many of the autoimmune conditions are much more prevalent in women of childbearing age.
Chronic lung disease in Singapore could be costing patients and health-care facilities US$128 million (S$165 million) a year, representing a significant burden to the public health system.
In the first local study on the economic cost of chronic obstructive pulmonary disease, or COPD, researchers have found that it costs the average patient US$2,000 each year to treat the ailment, more than three times that of asthma treatment. The bulk of the costs is due to hospital stays.
The researchers have called for more efforts to educate patients and health-care providers on the cost of the disease, and for its early detection and treatment.
Chronic obstructive pulmonary disease (COPD) is an umbrella term for two main disorders: emphysema and chronic bronchitis, diseases characterised by the obstruction to air flow in and out of the lungs.
Common symptoms are breathlessness, excessive production of sputum and a chronic cough. It is not merely a ‘smoker’s cough’, but an under-diagnosed, life-threatening lung disease. COPD is primarily caused by smoking, including passive smoking, and affects men and women almost equally.
It is curable, but treatment can stop its progress. COPD can be diagnosed by a simple test to measure how deeply a person can breathe and how fast air moves in and out of the lungs.
As such, there should be a cure for COPD if the process of autoantibodies can be stopped to prevent inflammation of the cells that causes COPD even though there is an irritant like smoking.
– Contributed by Oogle.
PARIS – A vaccine which revives a promising but long-abandoned path to thwart Alzheimer’s disease has cleared a key safety hurdle in human trials, researchers say.
In a small-scale test, the formula was found to be safe and primed the body’s frontline defences against protein deposits in the brain that are associated with the catastrophic disease.
Swedish doctors report the results in Wednesday’s issue of the journal Lancet Neurology, saying that the way is now open for wider trials.
The prototype vaccine, called CAD106, is a new exploration of traditional vaccine engineering.
In this approach, the pathogen that causes a disease is used to teach the immune system to identify an intruder and attack it.
In Alzheimer’s, one of the enemies is a toxic protein called amyloid beta peptide, which accumulates in plaques in the brain, although exactly how it works remains unclear.
A decade ago, doctors launched a first attempt at an amyloid beta vaccine, called AN1792.
But they were forced to abandon it at the second of the three-phase trial process after six per cent of the volunteers fell ill with meningoencephalitis, an inflammation of the brain.
The suspected reason was that AN1792 activated white blood cells called T cells that attacked the brain tissue.
The new vaccine uses a smaller fragment of the protein and combines it with a booster, called an adjuvant, intended to prevent T-cell activation.
After lengthy trials in the lab, a team led by Bengt Winblad of the Karolinska Institutet’s Alzheimer’s Disease Research Centre, tested the vaccine on 46 volunteers aged 50 to 80, diagnosed with mild to moderate Alzheimer’s.
A “control” group of 12 patients received a harmless formula, called a placebo, as a comparison.
The group was studied over 52 weeks and given a follow-up examination two years later.
Eighty-two per cent of the patients who received CAD106 developed antibodies, a sign that the immune defences had responded to the dangerous protein.
Overall, nine patients had episodes of ill health during the trial, but investigations showed these were unrelated to the drug, and none entailed meningoencephalitis.
The next step after this Phase 1 safety trial should be a larger test, possibly with modifications of the dose, to see if the vaccine works, says the study.
Around 26 million people around the world have Alzheimer’s, which remains an incurable and progressive disease characterised by memory loss and dementia.
The toll by 2050 is likely to be 115 million, according to figures cited in the journal.