dementia

Researchers find new drug may improve memory in people with moderate Alzheimer’s
March 14, 2013 by Sue
From the American Academy of Neurology press release via EurekAlert!:

A new drug may improve memory problems in people with moderate Alzheimer’s disease, according to a phase IIa study released today that will be presented at the American Academy of Neurology’s 65th Annual Meeting in San Diego, March 16 to 23, 2013. The drug is called ORM-12741.

The drug is the first to target a specific subtype of adrenergic receptors (alpha-2C) in the brain, which are believed to be involved in modulation of brain functions under stressful conditions, or the “fight or flight” response. For the clinical trial, 100 people with moderate Alzheimer’s disease were randomly given either 30 to 60 milligrams or 100 to 200 milligrams of ORM-12741 or matching placebo pill twice a day for three months as add-on therapy to a cholinesterase drug. Additionally, use of memantine was allowed. These are the other Alzheimer drugs currently on the market. Neither the researchers nor the participants knew which treatments participants were receiving.

After three months, researchers retested several aspects of the participants’ memory and behavior. Those who took ORM-12741 tested higher on the tests of memory compared to those who received the placebo pill. At three months, the memory scores for those who received the placebo pill had worsened by 33 percent, whereas the scores improved by 4 percent for those who took ORM-12741.

“Currently, there are still only a handful of Alzheimer’s drugs on the market and they have only moderate effects on the symptoms of the disease,” said study author Juha Rouru, MD, of Orion Pharma in Turku, Finland. “Anytime you have a drug that targets a new pathway in the brain and shows effectiveness in clinical trials, it is exciting.”

It is estimated that 13.8 million people will have Alzheimer’s disease by 2050.

Category: Memory, NeuroscienceTags: Alzheimer's, brain, cognition, dementia | Comments (0)
Researchers identify possible treatment window for memory problems
March 6, 2013 by Ashley
From the American Academy of Neurology press release via HealthCanal:

Researchers have identified a possible treatment window for plaques in the brain that are thought to cause memory loss in diseases such as Alzheimer’s, according to a new study published in the February 27, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Our study suggests that plaques in the brain that are linked to a decline in memory and thinking abilities, called beta amyloid, take about 15 years to build up and then plateau,” said Clifford R. Jack, Jr., MD, with the Mayo Clinic in Rochester, Minn.

For the study, 260 people between the ages of 70 and 92 underwent two or more brain scans over an average of 1.3 years that measured plaque buildup in the brain. Of the participants, 78 percent did not have impaired thinking abilities or memory at the start of the study.

The study found that the rate of buildup accelerates initially, then slows down before plateauing at high levels. For example, lower rates of plaque buildup were found in both people who had low and high levels of the plaques at the start of the study while the rate of plaque accumulation was highest in participants with mid-range levels at the start of the study.

The study also found that the rate of buildup of plaques was more closely tied to the total amount of amyloid plaques in the brain than other risk factors, such as the level of cognitive impairment, age and the presence of the APOE gene, a gene linked to Alzheimer’s disease.

“Our results suggest that there is a long treatment window where medications may be able to help slow buildup of the amyloid plaques that are linked to cognitive decline,” said Jack. “On the other hand, trying to treat the plaque buildup after the amyloid plaque load has plateaued may not do much good.”

The study was supported by the National Institutes of Health, National Institute on Aging and General Electric Corporation.

Category: Aging, Memory, NeuroscienceTags: Alzheimer's, brain, cognition, dementia, neurology | Comments (0)
Study suggests green tea, red wine extracts interrupt Alzheimer’s pathway
February 21, 2013 by Ashley
From the University of Leeds press release via EurekAlert!:

Natural chemicals found in green tea and red wine may disrupt a key step of the Alzheimer’s disease pathway, according to new research from the University of Leeds.

In early-stage laboratory experiments, the researchers identified the process which allows harmful clumps of protein to latch on to brain cells, causing them to die. They were able to interrupt this pathway using the purified extracts of EGCG from green tea and resveratrol from red wine.

The findings, published in the Journal of Biological Chemistry, offer potential new targets for developing drugs to treat Alzheimer’s disease, which affects some 800,000 people in the UK alone, and for which there is currently no cure.

“This is an important step in increasing our understanding of the cause and progression of Alzheimer’s disease,” says lead researcher Professor Nigel Hooper of the University’s Faculty of Biological Sciences. “It’s a misconception that Alzheimer’s is a natural part of ageing; it’s a disease that we believe can ultimately be cured through finding new opportunities for drug targets like this.”

Alzheimer’s disease is characterised by a distinct build-up of amyloid protein in the brain, which clumps together to form toxic, sticky balls of varying shapes. These amyloid balls latch on to the surface of nerve cells in the brain by attaching to proteins on the cell surface called prions, causing the nerve cells to malfunction and eventually die.

“We wanted to investigate whether the precise shape of the amyloid balls is essential for them to attach to the prion receptors, like the way a baseball fits snugly into its glove,” says co-author Dr Jo Rushworth. “And if so, we wanted to see if we could prevent the amyloid balls binding to prion by altering their shape, as this would stop the cells from dying.”

The team formed amyloid balls in a test tube and added them to human and animal brain cells. Professor Hooper said: “When we added the extracts from red wine and green tea, which recent research has shown to re-shape amyloid proteins, the amyloid balls no longer harmed the nerve cells. We saw that this was because their shape was distorted, so they could no longer bind to prion and disrupt cell function.

“We also showed, for the first time, that when amyloid balls stick to prion, it triggers the production of even more amyloid, in a deadly vicious cycle,” he added.

Professor Hooper says that the team’s next steps are to understand exactly how the amyloid-prion interaction kills off neurons.

“I’m certain that this will increase our understanding of Alzheimer’s disease even further, with the potential to reveal yet more drug targets,” he said.

Dr Simon Ridley, Head of Research at Alzheimer’s Research UK, the UK’s leading dementia research charity, which part-funded the study, said: “Understanding the causes of Alzheimer’s is vital if we are to find a way of stopping the disease in its tracks. While these early-stage results should not be a signal for people to stock up on green tea and red wine, they could provide an important new lead in the search for new and effective treatments. With half a million people affected by Alzheimer’s in the UK, we urgently need treatments that can halt the disease – that means it’s crucial to invest in research to take results like these from the lab bench to the clinic.”

Category: Aging, Health, NeuroscienceTags: Alzheimer's, brain, dementia, food, nutrition | Comments (0)
Study suggests consuming omega 3-rich complementary diet may help prevent onset of dementia
February 12, 2013 by Ashley
From the Universidad de Navarra press release via HealthCanal:

Researchers at the University of Navarra are carrying out a study the goal of which is to evaluate the consumption of omega 3 fatty acid-rich complementary diet as a protector factor against the onset of dementia.

“It could turn out to be a highly effective and acceptable preventative measure against the onset of this illness in elderly institutionalised patients with slight cognitive deterioration”, pointed out the authors, scientists at the Department of Preventive Medicine and Public Health at the University.

More than 24 million people throughout the world suffer from dementia, a figure which is likely to double every 20 years to reach more than 80 million by 2040. “The absence of curative treatment means that strategies for preventing the onset of dementia have special importance in the Public Health field”, stated Ms Maira Bes-Rastrollo, one of the research leaders.

Evaluation of cognitive and functional state

Ms. Maira Bes-Rastrollo highlights the fact that no random test has so far been undertaken in the primary prevention of this type of elderly patients: “Currently, we are at the stage of recruiting participants and in their basic evaluation”.

Thus, in order to carry out the research, two groups will be selected: one for intervention and who will have an omega 3 fatty acid-rich supplement added to their diet thrice-daily; the second is a control group, who will be administered a placebo. Both groups will have their cognitive and functional state evaluated at the start of the study and then again after a year, using a number of different scales which enable determining if there has been any improvement in this time. The methodology used to this end includes: Lobo’s Mini-Mental State Examination, Pfeiffer’s functional activity Short Portable Mental Status Questionnaire (SPMSQ), a verbal fluency test and the Clock Test.

Category: Aging, NeuroscienceTags: brain, cognition, dementia, food, nutrition | Comments (0)
Study suggests vitamin D3 and omega-3 fatty acids may help clear amyloid plaques associated with Alzheimer’s
February 11, 2013 by Ashley
From the UCLA press release by Rachel Champeau via ScienceDaily:

A team of academic researchers has pinpointed how vitamin D3 and omega-3 fatty acids may enhance the immune system’s ability to clear the brain of amyloid plaques, one of the hallmarks of Alzheimer’s disease.

In a small pilot study published in the Feb. 5 issue of the Journal of Alzheimer’s Disease, the scientists identified key genes and signaling networks regulated by vitamin D3 and the omega-3 fatty acid DHA (docosahexaenoic acid) that may help control inflammation and improve plaque clearance.

Previous laboratory work by the team helped clarify key mechanisms involved in helping vitamin D3 clear amyloid-beta, the abnormal protein found in the plaque. The new study extends the previous findings with vitamin D3 and highlights the role of omega-3 DHA.

“Our new study sheds further light on a possible role for nutritional substances such as vitamin D3 and omega-3 in boosting immunity to help fight Alzheimer’s,” said study author Dr. Milan Fiala, a researcher at the David Geffen School of Medicine at UCLA.

For the study, scientists drew blood samples from both Alzheimer’s patients and healthy controls, then isolated critical immune cells called macrophages from the blood. Macrophages are responsible for gobbling up amyloid-beta and other waste products in the brain and body.

The team incubated the immune cells overnight with amyloid-beta. They added either an active form of vitamin D3 called 1alpha,25–dihydroxyvitamin D3 or an active form of the omega-3 fatty acid DHA called resolvin D1 to some of the cells to gauge the effect they had on inflammation and amyloid-beta absorption.

Both 1alpha, 25-dihydroxyvitamin D3 and resolvin D1 improved the ability of the Alzheimer’s disease patients’ macrophages to gobble-up amyloid-beta, and they inhibited the cell death that is induced by amyloid-beta. Researchers observed that each nutrition molecule utilized different receptors and common signaling pathways to do this.

Previous work by the team, based on the function of Alzheimer’s patients’ macrophages, showed that there are two groups of patients and macrophages. In the current study, researchers found that the macrophages of the Alzheimer’s patients differentially expressed inflammatory genes, compared with the healthy controls, and that two distinct transcription patterns were found that further define the two groups: Group 1 had an increased transcription of inflammatory genes, while Group 2 had decreased transcription. Transcription is the first step leading to gene expression.

“Further study may help us identify if these two distinct transcription patterns of inflammatory genes could possibly distinguish either two stages or two types of Alzheimer’s disease,” said study author Mathew Mizwicki, an assistant researcher at the David Geffen School of Medicine at UCLA.

While researchers found that 1alpha,25-dihydroxyvitamin D3 and resolvin D1 greatly improved the clearance of amyloid-beta by macrophages in patients in both groups, they discovered subtleties in the effects the two substances had on the expression of inflammatory genes in the two groups. In Group 1, the increased-inflammation group, macrophages showed a decrease of inflammatory activation; in Group 2, macrophages showed an increase of the inflammatory genes IL1 and TLRs when either 1alpha,25-Dihydroxyvitamin D3 or resolvin D1 were added.

More study is needed, Fiala said, but these differences could be associated with the severity of patients’ nutritional and/or metabolic deficiencies of vitamin D3 and DHA, as well as the omega-3 fatty acid EPA (eicosapentaenoic acid).

“We may find that we need to carefully balance the supplementation with vitamin D3 and omega-3 fatty acids, depending on each patient in order to help promote efficient clearing of amyloid-beta,” Fiala said. “This is a first step in understanding what form and in which patients these nutrition substances might work best.”

According to Fiala, an active (not oxidized) form of omega-3 DHA, which is the precursor of the resolvin D1 used in this study, may work better than more commercially available forms of DHA, which generally are not protected against the oxidation that can render a molecule inactive.

The next step is a larger study to help confirm the findings, as well as a clinical trial with omega-3 DHA, the researchers said.

The Alzheimer’s Association contributed to the initial phase of the study. Fiala is a consultant for the Smartfish Company that is producing a drink with an active form of omega-3 DHA.

Additional study authors include Guanghao Liu, Larry Magpantay, James Sayre, Avi Siani, Michelle Mahanian, Rachel Weitzman, Eric Hayden, Mark J. Rosenthal, Ilka Nemere, John Ringman and David B. Teplow.

Category: Aging, Health, NeuroscienceTags: Alzheimer's, brain, cognition, dementia, food, nutrition | Comments (0)
Treatment to prevent Alzheimer’s moves a step closer
February 9, 2013 by Ashley
From the Lancaster University press release via HealthCanal:

A new drug to prevent the early stages of Alzheimer’s disease could enter clinical trials in a few years’ time according to scientists.

Alzheimer’s is the most common type of dementia, which currently affects 820,000 people in the UK, with numbers expected to more than double by 2050. One in three people over 65 will die with dementia.

The disease begins when a protein called amyloid-? (A?) starts to clump together in senile plaques in the brain, damaging nerve cells and leading to memory loss and confusion.

Professor David Allsop and Dr Mark Taylor at Lancaster University have successfully created a new drug which can reduce the number of senile plaques by a third, as well as more than doubling the number of new nerve cells in a particular region of the brain associated with memory. It also markedly reduced the amount of brain inflammation and oxidative damage associated with the disease.

The drug was tested on transgenic mice containing two mutant human genes linked to inherited forms of Alzheimer’s, so that they would develop some of the changes associated with the illness. The drug is designed to cross the blood-brain barrier and prevent the A? molecules from sticking together to form plaques.

Professor Allsop, who led the research and was the first scientist to isolate senile plaques from human brain, said: “When we got the test results back, we were highly encouraged. The amount of plaque in the brain had been reduced by a third and this could be improved if we gave a larger dose of the drug, because at this stage, we don’t know what the optimal dose is.”

The drug needs to be tested for safety before it can enter human trials, but, if it passes this hurdle, the aim would be to give the drug to people with mild symptoms of memory loss before they develop the illness.

“Many people who are mildly forgetful may go on to develop the disease because these senile plaques start forming years before any symptoms manifest themselves. The ultimate aim is to give the drug at that stage to stop any more damage to the brain, before it’s too late.”

The other researchers include groups led by Prof. Christian Hölscher at Ulster University, who conducted the mouse studies, and Prof. Massimo Masserini at University of Milano-Bicocca, Italy, who measured the ability of the drug to bind to A?.

Support for the research was given by Alzheimer’s Research UK, and the results are published in the open access journal PLOS ONE.

Dr Eric Karran, Director of Research at Alzheimer’s Research UK, said: “We are pleased to have supported this study, which represents the first step to developing much-needed new treatments to fight Alzheimer’s. These are promising early-stage results, and several years more work will be required to assess the potential of this approach. For science like this to make a real difference to people’s lives, we must continue to invest in research.”

Category: Health, NeuroscienceTags: Alzheimer's, brain, dementia | Comments (0)
Researchers identify stress hormone produced during exercise that may slow memory loss in Alzheimer’s
February 5, 2013 by Ashley
From the University of Nottingham press release via HealthCanal:

Keeping active can slow down the progression of memory loss in people with Alzheimer’s disease, a study has shown. A team of researchers from The University of Nottingham has identified a stress hormone produced during moderate exercise that may protect the brain from memory changes related to the disease.

The work, funded by Research into Ageing (Age UK) and the University and published in the Journal of Alzheimer’s Disease, may also explain why people who are susceptible to stress are at more risk of developing the disease.

Alzheimer’s disease is the most common cause of dementia affecting almost 500,000 people in the UK, the majority of who are over the age of 65. Symptoms can include memory loss, mood changes and problems with communicating and reasoning.

There is no cure for Alzheimer’s and, although there are a few treatments available that can reduce the symptoms in some people, they cannot halt the progression of the disease.

Increasingly, there is evidence that physical and mental activity can reduce people’s chances of developing the disease or can slow down it’s progression but up until now it has been unclear how this happens.

The Nottingham team, led by Dr Marie-Christine Pardon in the School of Biomedical Sciences, has discovered that the stress hormone CRF — or corticotrophin-releasing factor — may have a protective effect on the brain from the memory changes brought on by Alzheimer’s disease.

CRF is most associated with producing stress and is found in high levels in people experiencing some forms of anxiety and depressive diseases. Normal levels of CRF, however, are beneficial to the brain, keeping the mental faculties sharp and aiding the survival of nerve cells. Unsurprisingly then, studies have shown that people with Alzheimer’s disease have a reduced level of CRF.

The researchers used an experimental drug to prevent the hormone from binding to a brain receptor called CRFR1 in mice with Alzheimer’s disease that were free from memory impairments, therefore blocking the effects of the hormone.

They discovered that the mice had an abnormal stress response with reduced anxiety but increased behavioural inhibition when confronted by a stressful situation — in this case being placed in a new environment — and this is was due to the abnormal functioning of the CRFR1. This abnormal stress response before the onset of symptoms may explain why people susceptible to stress are more at risk of developing Alzheimer’s.

Dr Pardon and her team also found that interrupting the hormone from binding on to the CRFR1 receptor blocked the improvement of memory normally promoted by exercise. However, in mice with Alzheimer’s a repeated regime of moderate exercise restored the normal function of the CRF system allowing its memory enhancing effects. The results are in line with the idea that regular exercise is a means of improving one’s ability to deal with everyday stress in addition to keeping mental abilities keen.

Finally, their study showed that the switching on of this particular brain receptor during exercise increased the density of synapses, which makes the connection between nerve cells, the loss of which is thought to be responsible for the early memory loss seen in Alzheimer’s patients.

Dr Pardon said: “This is the first time that researchers have been able to identify a brain process directly responsible for the beneficial effects of exercise in slowing down the progression of the early memory decline characteristics of Alzheimer’s disease.

“Overall, this research provides further evidence that a healthy lifestyle involving exercise slows down the risk of Alzheimer’s disease and opens avenues for the new interventions targeting the altered CRFR1 function associated with the early stages of the disease.”

An early online version of the paper — Corticotropin-Releasing Factor Receptor 1 Activation During Exposure to Novelty Stress Protects Against Alzheimer’s Disease-Like Cognitive Decline in A?PP/PS1 Mice — detailing the findings has been published online at http://iospress.metapress.com/content/75m787746365k55g/?p=8dd6b9cb0afd4f2ebc9937ffbc7fc985&pi=0

Category: Health, Memory, NeuroscienceTags: Alzheimer's, brain, dementia, exercise | Comments (0)
First guidelines for brain amyloid imaging in Alzheimer’s released
January 30, 2013 by Ashley
From the Society of Nuclear Medicine press release via EurekAlert!:
Only recently has it become possible to create high-quality images of the brain plaques characteristic of Alzheimer’s disease in living people through positron emission tomography (PET). Even so, questions remain about what can be learned from these PET images and which people should have this test.

To provide guidance for physicians, individuals and families affected by Alzheimer’s, and the public, the Society of Nuclear Medicine and Molecular Imaging (SNMMI) and the Alzheimer’s Association have jointly published the first criteria for the appropriate use of this imaging technology to aid in the diagnosis of people with suspected Alzheimer’s disease. The criteria were published online today as an article “in press” by Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association and “ahead of print” in The Journal of Nuclear Medicine.

“Our primary goal is to provide healthcare practitioners with the information and options available to provide patients with the best possible diagnosis and care in a cost effective manner,” said Maria Carrillo, Ph.D., Alzheimer’s Association vice president of Medical and Scientific Relations.

Appropriate Use Criteria (AUC) for Brain Amyloid Imaging with PET in Alzheimer’s

While elevated beta amyloid plaques are one of the defining pathologic features of Alzheimer’s, many elderly people with normal cognition also have elevated levels of these plaques, as do people with conditions other than Alzheimer’s dementia. Therefore, the potential clinical use of amyloid PET requires careful consideration so that its proper role may be identified.

To develop the new criteria, the Alzheimer’s Association and SNMMI assembled an Amyloid Imaging Taskforce (AIT) consisting of dementia and imaging experts to review the scientific literature and develop consensus recommendations for the clinical use of this promising new technology.

The AIT concluded that amyloid imaging could potentially be helpful in the diagnosis of people with cognitive impairment when considered along with other clinical information, and when performed according to standardized protocols by trained staff. In addition, they emphasized that the decision whether or not to order amyloid imaging should be made only after a comprehensive evaluation by a physician experienced in the assessment and diagnosis of cognitive impairment and dementia, and only if the presence or absence of amyloid would increase certainty in the diagnosis and alter the treatment plan.

According to the AIT, appropriate candidates for amyloid PET imaging include:
- Those who complain of persistent or progressive unexplained memory problems or confusion and who demonstrate impairments using standard tests of cognition and memory.
- Individuals meeting tests for possible Alzheimer’s, but who are unusual in their clinical presentation.
- Individuals with progressive dementia and atypically early age of onset (before age 65).
Inappropriate candidates for amyloid PET imaging include:
- Those who are age 65 or older and meet standard definitions and tests for Alzheimer’s, since a positive PET scan would provide little added value.
- Asymptomatic people or those with a cognitive complaint but no clinical confirmation of impairment.
Amyloid PET imaging is also inappropriate:
- As a means of determining the severity of dementia.
- When requested solely based on a family history of dementia or presence of other risk factors for Alzheimer’s, such as the ApoE-e4 gene.
- As a substitute for genetic testing for mutations that cause Alzheimer’s.
- For non-medical reasons, such as insurance, legal or employment decisions.
“As amyloid imaging becomes more prevalent in clinical settings, medical professionals must understand how to appropriately utilize the test,” said Frederic H. Fahey, D.Sc., SNMMI president. “Neurology and dementia experts should order the test only when appropriately indicated, and nuclear medicine and molecular imaging professionals must ensure they have been adequately trained to interpret the results of the scan. Working together, we hope that the information garnered from amyloid PET imaging will aid in diagnosis and play a pivotal role in the development of new treatments for Alzheimer’s.”

The taskforce acknowledged that the healthcare provider makes the ultimate judgment regarding the care of each patient. The AIT sought to assist this process and identified the following general sequence of events for the use of amyloid PET according to the new criteria:
1. Evaluation by a dementia expert to assess the need for diagnostic testing, possibly to include amyloid PET if the AUC are met.
2. Referral to a qualified provider of amyloid PET services.
3. Performance, interpretation and reporting of the amyloid PET scan according to established standards.
4. Incorporation of the PET result into the clinical assessment process.
5. Disclosure of the PET result by the clinician to the patient and caregivers, along with discussion of the result and its management consequences.
Although identifying potential benefits, the AIT concluded that amyloid PET results will not constitute and is not equivalent to a clinical diagnosis of Alzheimer’s disease dementia. They said that imaging is only one tool among many that clinicians should use judiciously to manage patients, and that amyloid PET imaging does not substitute for a careful history and examination.

“Because both dementia care and amyloid PET technology are in active development, these new appropriate use criteria will require periodic reassessment and updating,” Carrillo said.

PET Amyloid Imaging in Alzheimer’s – An Overview

PET uses radiopharmaceuticals (radioactive drugs) to produce three-dimensional functional images of the brain or other body part. In amyloid PET imaging, the radiopharmaceutical is introduced into the body by injection into a vein and binds specifically to the amyloid protein, enabling visualization of areas in the brain where amyloid has clumped together into plaques. One of the new PET compounds was approved for general use by the U.S. Food and Drug Administration in April 2012.
- If a person with dementia does not have amyloid buildup in their brain, then the cause of the dementia is very likely to be something other than Alzheimer’s disease. Other causes of dementia include: strokes, thyroid problems, drug interactions, chronic alcoholism, and vitamin deficiencies.
- If an amyloid imaging PET scan shows that a person with memory impairment has amyloid buildup in their brain, this increases the likelihood that the memory impairment is caused by Alzheimer’s disease, but it remains a likelihood, not a certainty.
- If a person without memory complaints or impairment has amyloid buildup, it does not necessarily mean that they will develop Alzheimer’s. Many people have amyloid in their brains but are cognitively normal. More research is needed to understand the significance of amyloid plaques in this population.
Amyloid imaging is not covered by insurance at this time, and costs for the scan are “out of pocket.” While costs of amyloid PET are not yet established, and PET costs in general can vary depending upon location, other PET scans are known to cost between $1,000 and $3,000, or more.

Nonetheless, the AIT concluded that the proven sensitivity and specificity of the new radiopharmaceuticals for brain amyloid and the known association between brain beta amyloid deposition and Alzheimer’s suggest these new radiopharmaceuticals could potentially be helpful in the workup and diagnosis of patients with cognitive impairment.
Category: NeuroscienceTags: Alzheimer's, brain, cognition, dementia | Comments (0)
Study links passive smoking to increased risk of severe dementia
January 10, 2013 by Sue
From the King’s College London press release:

An international study by scientists in China, the UK and USA has found a link between passive smoking and syndromes of dementia.

The study of nearly 6,000 people in five provinces in China reveals that people exposed to passive smoking have a significantly increased risk of severe dementia syndromes.

Passive smoking, also known as ‘second-hand’ smoke or environmental tobacco smoke (ETS), is known to cause serious cardiovascular and respiratory diseases, including coronary heart disease and lung cancer. However, until now it has been uncertain whether ETS increases the risk of dementia, mainly due to lack of research. Previous studies have shown an association between ETS and cognitive impairment, but this is the first to find a significant link with dementia syndromes.

The study, published in Occupational and Environmental Medicine, is a collaboration between scientists at King’s College London and Anhui Medical University, China, along with colleagues in the UK and USA.

According to the World Health Organization (WHO), nearly 80 percent of the more than one billion smokers worldwide live in low- and middle-income countries, where the burden of tobacco-related illness and death is heaviest; but only 11 percent of the world’s population are protected by comprehensive smoke-free laws.

China is the largest consumer of tobacco in the world, with 350 million smokers. Since 2006, the Chinese government has actively promoted the introduction of smoke-free environments in hospitals, schools, on public transport and in other public places, but implementation has not been widespread.

Recent data show that the prevalence of passive smoking is still high, with over 50 percent of people exposed to environmental tobacco smoke on a daily basis. China also has the highest number of dementia sufferers in the world, with increasing rates of new cases as the population ages.

Dr Ruoling Chen, senior lecturer in public health from King’s College London, and colleagues interviewed 5,921 people aged over 60 in the rural and urban communities of Anhui, Guangdong, Heilongjiang, Shanghai and Shanxi to characterise their levels of ETS exposure, smoking habits and assess levels of dementia syndromes.

They found that 10 percent of the group had severe dementia syndromes. This was significantly related to exposure level and duration of passive smoking. The associations with severe syndromes were found in people who had never smoked and in former and current smokers.

The data from the Anhui cohort, which were collected at baseline in 2001-03 for dementia syndromes and in the follow up in 2007-08 for ETS exposure and dementia, further excluded the possibility that dementia syndromes caused people to be more exposed to environmental tobacco smoke.

Dr Ruoling Chen, also a visiting professor at Anhui Medical University said: ‘Passive smoking should be considered an important risk factor for severe dementia syndromes, as this study in China shows. Avoiding exposure to ETS may reduce the risk of severe dementia syndromes.

‘China, along with many other countries, now has a significantly ageing population, so dementia has a significant impact not only on the patients but on their families and carers. It’s a huge burden on society.’

The findings from this study, together with a second recent study by Chen and colleagues published in Alzheimer’s & Dementia on the links between passive smoking and Alzheimer’s disease, strengthen the case for public health measures to protect people from exposure to environmental tobacco smoke.

‘At present, we know that about 90 percent of the world’s population live in countries without smoke-free public areas. More campaigns against tobacco exposure in the general population will help decrease the risk of severe dementia syndromes and reduce the dementia epidemic worldwide.’

He added: ‘The increased risk of severe dementia syndromes in those exposed to passive smoking is similar to increased risk of coronary heart disease – suggesting that urgent preventive measures should be taken, not just in China but many other countries.’

Category: Aging, Health, MemoryTags: Alzheimer's, dementia, smoking | Comments (0)
Risk genes for Alzheimer’s and mental illness linked to brain changes at birth
January 8, 2013 by Sue
From the UNC School of Medicine press release via HealthCanal:

Some brain changes that are found in adults with common gene variants linked to disorders such as Alzheimer’s disease, schizophrenia, and autism can also be seen in the brain scans of newborns.

“These results suggest that prenatal brain development may be a very important influence on psychiatric risk later in life,” said Rebecca C. Knickmeyer, PhD, lead author of the study and assistant professor of psychiatry in the University of North Carolina School of Medicine. The study was published online by the journal Cerebral Cortex on Jan. 3, 2013.

The study included 272 infants who received MRI scans at UNC Hospitals shortly after birth. The DNA of each was tested for 10 common variations in 7 genes that have been linked to brain structure in adults. These genes have also been implicated in conditions such as schizophrenia, bipolar disorder, autism, Alzheimer’s disease, anxiety disorders and depression.

For some polymorphisms – such as a variation in the APOE gene which is associated with Alzheimer’s disease – the brain changes in infants looked very similar to brain changes found in adults with the same variants, Knickmeyer said. “This could stimulate an exciting new line of research focused on preventing onset of illness through very early intervention in at-risk individuals.”

But this was not true for every polymorphism included in the study, said John H. Gilmore, MD, senior author of the study and Thad & Alice Eure Distinguished Professor and Vice Chair for Research and Scientific Affairs in the UNC Department of Psychiatry.

For example, the study included two variants in the DISC1 gene. For one of these variants, known as rs821616, the infant brains looked very similar to the brains of adults with this variant. But there was no such similarity between infant brains and adult brains for the other variant, rs6675281.

“This suggests that the brain changes associated with this gene variant aren’t present at birth but develop later in life, perhaps during puberty,” Gilmore said.

“It’s fascinating that different variants in the same gene have such unique effects in terms of when they affect brain development,” said Knickmeyer.

In addition to Knickmeyer and Gilmore, authors of the study were Jiaping Wang, PhD; Hongtu Zhu, PhD; Xiujuan Geng, PhD; Sandra Woolson, MPh; Robert M. Hamer, PhD; Thomas Konneker, BA; Weili Lin, PhD; and Martin Styner, PhD. All are at UNC except Konneker, who was at UNC but is now a PhD student at the University of California, Santa Cruz.

The study was funded by grants from the National Institutes of Health.

Category: NeuroscienceTags: Alzheimer's, brain, dementia, mental health | Comments (0)