A Copenhagen-based chemist has taken out a U.S. patent for a drug that can make previously resistant bacteria newly responsive to antibiotics. Many strains of bacteria have the ability to mutate, adapting defenses against whatever antibiotic is used against them before the drug has the ability to become fully effective. Of particular concern is multidrug resistant tuberculosis (MDR-TB) that quickly adapts to treatments, gradually becoming resistant to all available forms.
Many years ago, bacterial infections were major global problems for all societies. The discovery of penicillin reduced the danger of bacterial infection and raised the quality of life and hygiene for nearly all people worldwide. Since then, however, many strains of bacteria have developed resistance to penicillin, requiring the development of newer antibiotic treatments- with time, those too became inadequate and current bacterial infections elude even the most esoteric of treatments.
Jørn Bolstad Christensen, the chemist responsible for devising a method around this resistance, has produced a substance that blocks the bacteria’s ability to resist treatment. Essentially, if the bacterium is resistant to the treatment, it will ingest and then quickly excrete the substance before it has a chance to take effect. Christensen’s chemical closes the pumping mechanism by which the bacteria can do this, leaving the drug inside the bacteria for enough time for it to be effective.
At the moment, tests have been very positive and Christensen is waiting for funding to develop a marketable product for the industrialized world. Because the anti-resistance medication is in fact an isomer of the already widely available drug Thioridazin, it should be possible to sidestep the necessary pharmaceutical approval and move directly towards commercialization.
If an investor does not show interest in the anti-resistance drug, Christensen reports that it is likely he will donate it to an NGO capable of delivering the drug to poor nations that suffer from drug-resistant problems.
A recent development at the University of Illinois in Chicago has produced a type of nanoparticle drug-delivery system that allows anti-inflammatory drugs to only target the immune cells that have gone out of control without damaging the nearby healthy cells.
The nanoparticles are comprised of tiny bits of a specific protein designed to connect to and bind with receptors only found on neutrophils – the immune cell responsible for chronic inflammatory responses.
Published on February 23, 2014 in Nature Nanotechnology, the university’s findings report that these specific proteins can bind with and compromise the buildup of unwanted neutrophils in the human body. The mechanism for unwanted buildup is already well-understood: during a normal immune response, neutrophils respond to signals from damaged blood vessels and then accumulate and engulf the nearby bacteria and foreign matter, preventing infection.
What happens during chronic inflammatory response is that some of these neutrophils go out of control and begin sticking to the blood vessel walls, themselves, and everything nearby, causing a blockage that contributes to tissue damage. In acute lung injury, for example, this can lead to trouble breathing that currently shows a 50% mortality rate.
Current anti-inflammatory drugs are very blunt, targeting the entire affected area and producing numerous unwanted side effects. By identifying the unique protein surface of the neutrophils and attaching the anti-inflammatory drug to the resulting nanoparticle, these drugs can be designed to neutralize only the cells that are causing problems.
The researchers responsible call this a, “Trojan Horse” tactic that tricks the troublesome neutrophils into accepting the bond with the anti-inflammatory agent while leaving the well-behaved ones alone to continue doing their job. These findings will lead to more effective medication for inflammatory response and a vastly decreased mortality rate among patients with these kinds of problems.
A recent study on the antidepressant citalopram (sold under the brand name of Cipramil or Celexa) showed significant agitation relief for Alzheimer’s patients. Current treatments for agitation require the use of dangerous antipsychotic drugs that have been shown to increase the patient’s risk of stroke, heart attack, and death.
The study was reported in the February 19 issue of the Journal of the American Medical Association. It details the agitation symptoms in 186 Alzheimer’s patients that included emotional distress, aggression, excessive movement, disinhibition and irritability. None of these patients experienced adequate relief from these symptoms through non-medical therapy, and some of them also failed to react to treatment using antipsychotics.
At the conclusion of the study, 40% of the patients who took citalopram reported “considerable relief” from their agitation symptoms while only 26% of the placebo-fed control group did the same. It is important to note that the caretakers responsible for these 26% reported less stress than usual. The important causal relationship between caretaker stress and Alzheimer’s patient symptom relief is well known and was factored into this study’s results.
Side effects related to the use of citalopram are small but measurable: many had slightly decreased cognitive function and this could represent an important tradeoff for patients. Of even greater concern is that these patients showed an increased measure of abnormal heart function, which may lead to higher risk of heart attack. Knowing that the antipsychotic alternative also increases heart attack risk, however, leaves little in the way of other options for patients with weak hearts.
Further tests will determine whether lower doses can produce the desired effects while reducing the risk of cognitive or cardiac malfunction. At the moment, evidence points towards the new use of a medication that, while not perfect, is safer than any existing alternative and just as effective.