COPD Linked to Cognitive Impairment, Memory Loss

A study by the Mayo Clinic has found that people with chronic obstructive pulmonary disease (COPD) are about twice as likely to develop mild cognitive impairment (MCI) -- and chances are that it will include memory loss.

Researchers looked at about 2,000 people 70-89 years old in the Mayo Clinic Study on Aging. About 1,600 were cognitively normal, 317 had mild cognitive impairment and overall, about 288 had COPD. COPD was found to be associated with almost two-fold higher odds of MCI, and the odds get worse the longer someone has COPD. Rates were similar among men and women.

“COPD is reversible in early stages, especially in smokers,”  says study author Dr. Balwinder Singh. “These findings are important because they highlight the importance of COPD as a potential risk factor for MCI and will hopefully lead to early intervention to prevent incidence or progression.”

MCI is a stage between normal cognitive aging and dementia. People with mild cognitive impairment are at increased risk of progressing to dementia and Alzheimer’s disease.

COPD refers to a group of lung diseases that block airflow and make breathing difficult. Emphysema and chronic bronchitis are the two most common conditions that make up COPD. Chronic bronchitis is an inflammation of the lining of your bronchial tubes, which carry air to and from your lungs. Emphysema occurs when the air sacs (alveoli) at the end of the smallest air passages (bronchioles) in the lungs are gradually destroyed.

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Many COPD patients feel outlook is bleak; Researchers call for more education

(Source: Medwire News)

Researchers behind a global survey of chronic obstructive pulmonary disease (COPD) patients say that more must be done to educate patients about the disease and what to do during exacerbations.

The team, led by Neil Barnes from the London Chest Hospital, UK, surveyed patients from 14 countries and found that many seemed to have low expectations around disease control and were unaware of the importance of responding quickly to exacerbations.

Furthermore, the study highlighted the impact of COPD on patient quality of life, with many reporting they took a limited outlook on the future and feared the illness would curtail their life expectancy.

“By highlighting the fears and concerns of COPD patients, many of whom are of working age with financial and familial responsibilities, the survey draws attention to the need for better patient education regarding the severity of the disease, the importance of prompt treatment of exacerbations, and the treatment and lifestyle options available,” Barnes and team write in BMC Pulmonary Medicine.

Their study involved survey responses from 2000 patients with COPD, chronic bronchitis, and/or emphysema, who were categorized according to Medical Research Council (MRC) breathlessness score: 1231 (62%) were grades 1 or 2 and 769 (38%) were grades 3–5.

The team found that despite heavy healthcare use during the preceding 12 months, 69% of patients thought that their COPD was well-controlled.

“This type of mismatch is not unusual, and has been widely reported in studies of both COPD and asthma patients, suggesting low levels of expectation,” the authors comment.

Overall, 62% of patients in MRC 1 or 2 grades and 80% of patients in MRC grades 3 to 5 had experienced an exacerbation in the previous 12 months, with 52% of patients in the latter group requiring hospitalization.

However, 27% of patients did not contact their healthcare service during exacerbation, taking actions such as cutting down on smoking, resting, or increasing medication dosage instead. And, less than 60% said that they would take immediate action in response to an exacerbation.

Patients reported that COPD and exacerbations affected their quality of life and their ability to commit to future events, with 77% worried about their long-term health. Additionally, 38% of MRC 1 and 2 patients said they feared premature death due to COPD, as did 59% of MRC 3 to 5 patients.

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Inflammatory on and off switch identified for allergic asthma and COPD

Japanese researchers have made a new step toward understanding why—and how to stop—runaway inflammation for both chronic obstructive pulmonary disorder (COPD) and allergic asthma.

In a new report appearing in the August 2013 issue of The FASEB Journal scientists show that two receptors of an inflammatory molecule, called "leukotriene B4," play opposing roles in turning inflammation on and off for allergic asthma and COPD. The first receptor, called "BLT1," promotes inflammation, while the second receptor, called "BLT2," has a potential to weaken inflammation during an allergic reaction. This discovery also is important because until now, BLT2 was believed to increase inflammatory reaction.

"Leukotriene B4 levels are elevated in the airways of the patients with asthma and COPD, and the opposite role of BLT1 and BLT2 in allergic inflammation implies that drug development should target BLT1 and BLT2 differently," said Hiromasa Inoue, M.D., study author from the Department of Pulmonary Medicine at the Graduate School of Medical and Dental Sciences at Kagoshima University in Kagoshima, Japan. "We hope that better anti-asthma drugs or anti-COPD drugs will be produced in the future to treat millions of patients who suffer from severe asthma and COPD."

To make this discovery, scientists compared the allergic reactions in BLT2-gene deleted mice to those in normal mice. Then an allergic asthma reaction was provoked by inhalation of allergens. BLT2-gene deleted mice showed more inflammatory cells in the lung compared to normal mice. Without the BLT2 gene, lung allergic inflammation was stronger than that of normal mice. The production of interleukin-13, an important mediator of allergic inflammation from T lymphocytes, was increased in the group without the BLT2 gene. Results suggest that targeting these two receptors differently and/or separately could achieve vastly different outcomes. Conventional anti-leukotriene B4 drugs block both of the pathways induced by BLT1 and BLT2. By manipulating the specific target, it may be possible to develop more effective anti-leukotriene B4 drugs.

"This is one case where BLT isn't a sandwich! Distinguishing between BLT1 and BLT2 is an important step forward to developing more effective drugs for lung inflammation," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "Understanding the specific roles of these and other receptors allow researchers to identify new drug targets, which in turn can lead to new and more effective drugs."

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COPD study shows more than smokers affected; women, under 45's and non-smokers

Preliminary findings by the UCLA Center for Health Policy Research along with Survey Research Group and Public Health Institute (PHI) reveal that many people in California diagnosed with COPD have never smoked, are under the age of 45, and are women, providing a striking contrast to the perception that the disease is only a 'smokers' condition affecting men and older people

New data shows an estimated 1.1 million Californians, with nearly 200,000 in Los Angeles County, have been diagnosed with COPD.

"BREATHE LA (BLA) funded the UCLA research to fill a significant gap in the understanding of COPD's impact in California. We now know COPD prevalence in the state is more complex than many people realize," said Enrique Chiock, BLA President and CEO.

"COPD progressively destroys the lungs and has no cure. Mortality rates continue to rise, yet many people with COPD are undiagnosed or are unaware of the lifestyle changes needed to manage the condition and improve their quality of life," said leading pulmonologist Dr. Guy Soo Hoo, a former BLA Board Chair. "This data gives us hard numbers to show to policymakers and the medical community that we are in the midst of a public health crisis. The cost of COPD to our economy and to our healthcare industry needs to be mitigated through prevention, early diagnosis, and treatment."

According to National Institute of Health findings, despite nearly 140,000 annual COPD deaths, government funding for disease research and programs is dwarfed by funding for other diseases, such as AIDS/HIV. For example, funding for AIDS/HIV research and programs is nearly 30 times greater than that for COPD, even though COPD claims nearly 15 times as many lives each year.

BREATHE LA's advocacy focus is to raise awareness and promote solutions for the COPD crisis. BLA representatives recently discussed the data with Congressman Henry A. Waxman, D-California, a longtime advocate of lung health.

"The increase in COPD is yet another result of tobacco's harmful effects and the dangers of polluted air. COPD is now the third leading cause of death nationwide. An estimated 12 million Americans are diagnosed with the disease and another 12 million may be affected by the disease but are undiagnosed. Californians, especially those of us from Los Angeles, know firsthand how important it is to have clean air to breathe," Rep. Waxman said. "I will continue my ongoing efforts to address the primary causes of COPD - killer tobacco and dirty air. And, I am encouraged that organizations like BREATHE LA are passionate about doing the same."

The UCLA report, which will be released later this year, will be important for understanding how COPD is currently diagnosed and treated. For example, preliminary analyses show approximately one-third of those diagnosed with COPD never received a spirometry test, though this is the only approved method for diagnosis.

"COPD remains a significant public health burden. There is still ample room for improvement in adherence to primary prevention and treatment," said Dr. Ying-Ying Meng, lead author of the report and Co-Director, of the Chronic Disease Program at the UCLA Center for Health Policy Research. "Our findings highlight the need to incorporate prevention, early diagnosis and treatment strategies that aim at reducing activity limitations, emergency department visits and mortality due to COPD."

The preliminary data analysis will be discussed as part of BREATHE LA's "Living Well with COPD" Fourth COPD Conference on November 14 (World COPD Awareness Day) in Los Angeles. The Conference will feature presentations on approaches to address the disease, promoting prevention, early diagnosis, treatment and management. For more information about the conference and to register to attend, visit http://www.breathela.org/COPDConference2012 .

Researchers find genetic link between smoking, COPD

University of Iowa researchers have found what they believe is the first link between smoking and decreased expression of a new class of noncoding RNAs (microRNAs) in smokers’ immune cells.

“Only 20 percent of smokers get chronic obstructive pulmonary disease (COPD), but no one knows why,” says Martha Monick, Ph.D., professor of internal medicine at the UI Roy J. and Lucille A. Carver College of Medicine. “This discovery identifies changes in a new class of molecules, microRNAs, that might be driving gene expression that ultimately leads to COPD/emphysema and other smoking-related disorders.”

Additionally, Monick says the discovery identifies specific smoking altered microRNAs that may provide future therapeutic targets.

The study, which looks at microRNA and gene expression in lung immune cells,was published online recently in the journal PLoS ONE at dx.plos.org/10.1371/journal.pone.0044066. Monick is co-senior author with Mary Wilson, M.D., UI professor of internal medicine and microbiology. Joel Graff, PhD, a research scientist in Wilson’s laboratory, is primary author, and Thomas Gross, M.D., UI associate professor of internal medicine, is a co-author and oversees the clinical aspects of the research.

According to Monick, the new research identifies changes in microRNAs, a new class of gene expression regulators, in cells from smokers’ compared to nonsmokers' lungs. It is the first study to demonstrate significant down-regulation of these small noncoding RNAs (microRNAs) in lung macrophages from smokers. Macrophages are critical components of the innate immune system and changes in these cells are strongly linked to disease development.

In addition, the study links changes in a specific microRNA (miR-452) to increased production of a protein-degrading enzyme called MMP12, long associated with the development of COPD and emphysema. This research, she says, identifies a novel biological mechanism (changes in microRNA expression controlling disease relevant genes) that may be playing an important role in smoking-related diseases.

“We discovered the massive down-regulation of microRNAs with smoking and are continuing to study the mechanism of that down regulation. We are also working to identify specific microRNAs, like the one we have linked to MMP12, that alter expression of genes involved in smoking-related diseases." Monick says.

“Despite 50 years of accumulating knowledge on the health hazards of smoking, people continue to smoke. Every day approximately 4,000 people under the age of 18 pick up their first cigarette," Monick says.

“Research on the mechanism behind smoking-related diseases and identification of markers to identify high risk individuals remains critically important."