Archives for September 2014

Healthy Lifestyles Reduce the Incidence of Chronic Diseases and Dementia

PLoS One. 2013 Dec 9;8(12):e81877. doi: 10.1371/journal.pone.0081877. eCollection 2013.

Healthy lifestyles reduce the incidence of chronic diseases and dementia: evidence from the caerphilly cohort study.

Elwood P1, Galante J1, Pickering J1, Palmer S1, Bayer A1, Ben-Shlomo Y2, Longley M3, Gallacher J1.

Author information



Healthy lifestyles based on non-smoking, an acceptable BMI, a high fruit and vegetable intake, regular physical activity, and low/moderate alcohol intake, are associated with reductions in the incidence of certain chronic diseases, but to date there is limited evidence on cognitive function and dementia.


In 1979 healthy behaviours were recorded on 2,235 men aged 45-59 years in Caerphilly, UK. During the following 30 years incident diabetes, vascular disease, cancer and death were recorded, and in 2004 cognitive state was determined.


Men who followed four or five of the behaviours had an odds ratio (OR) and confidence intervals (CI) for diabetes, corrected for age and social class, of 0.50 (95% CI: 0.19, 1.31; P for trend with increasing numbers of healthy behaviours <0.0005). For vascular disease the OR was 0.50 (95% CI: 0.30, 0.84; P for trend <0.0005), and there was a delay in vascular disease events of up to 12 years. Cancer incidence was not significantly related to lifestyle although there was a reduction associated with non-smoking (OR: 0.65; 95% CI: 0.54, 0.79). All-cause mortality was reduced in men following four or five behaviours (OR 0.40; 95% CI: 0.24, 0.67; P for trend <0.005).

After further adjustment for NART, the OR for men following four or five healthy behaviours was 0.36 (95% CI: 0.12, 1.09; P for trend <0.001) for cognitive impairment, and 0.36 (95% CI: 0.07, 1.99; P for trend <0.02) for dementia. The adoption of a healthy lifestyle by men was low and appears not to have changed during the subsequent 30 years, with under 1% of men following all five of the behaviours and 5% reporting four or more in 1979 and in 2009.


A healthy lifestyle is associated with increased disease-free survival and reduced cognitive impairment but the uptake remains low.



Weight Loss in the Dementia Patient

Dear Readers:

I found this article, written for health care professionals, about weight loss in dementia patients. It contains some good information so I thought I would post it here for you.

Poor nutrition, dehydration, swallowing difficulties, and weight loss are serious issues. If your loved one is experiencing weight loss, or other health-related issue, please see a physician for diagnosis and treatment.

~ Best, Jennifer

( Dementia patients frequently lose weight regardless of whether they are cared for at home or in a long-term care facility. Weight loss can be distressing to family and hunger can cause agitation in the Alzheimer patient. Most Alzheimer patients lose weight for a variety of reasons and accurate diagnosis is the first step in an effective plan to maintain adequate body mass.

The clinician or family member must approach weight loss in a systematic way to identify simple correctable causes of weight loss.   Treatment teams should focus on fluid, fiber and calories in the dementia patients. Dementia patients need proper hydration, sufficient fiber to assure proper caloric function and sufficient quantities of food to maintain weight and nutrition.

Dementia can be divided into three stages early, middle and late. The causes of weigh loss in each phase may differ. The boundary between early and middle stage dementia is vague. Early stage patients are usually forgetful and sometimes anxious.   These patients function reasonably well with minimal supervision. Middle stage patients have multiple intellectual losses and need extensive assistance with daily living activities. Late stage patients have severe intellectual limitations and cannot care for themselves.

Early Stage

Early stage dementia patients usually maintain adequate body weight. Physical problems such as cancer, diabetes or thyroid disease should be considered in any mildly demented patient who is losing weight. Depression is common in early dementia and will result in weight loss as a result of anorexia. Early stage dementia patients should be capable of describing symptoms such dental problems, swallowing difficulties, abdominal pain etc., that cause patients to stop eating. These patients should maintain adequate fluid, fiber and nutrition.

 Middle Stage

Middle stage dementia patients frequently lose weight. Weight loss results in muscular weakness, falls, health problems, and other complications that lower the patient’s quality of life and complicate management.   Middle stage dementia

patients lose weight for three distinct reasons: (1) metabolic i.e., burning large number of calories, (2) physical/mechanical i.e., can’t consume enough food, and (3) psychiatric, i.e., not interested in eating.   The clinician should carefully evaluate patients to exclude medical causes (e.g., cancer, diabetes, thyroid disorder). Dementia patients frequently pace, wander, and are constantly in motion — a level of physical activity requiring increased numbers of calories. Dementia patients often burn more calories than cognitively intact elders.

Psychiatrically disturbed patients may be delusional about food and will not eat for fear of poisoning. Psychotic patients may be distracted during dining hours, refuse to enter the dining room because of voices or leave the table before completion of the meal. Psychotic patients can be distracted by the noise in a dining hall. Depressed patients will lose their appetite and stop eating.

Dementia patients lose the ability to recognize food. Alzheimer patients may sit at the table and not eat unless utensils are placed in their hands and they are encouraged to eat. Many patients develop feeding apraxia (i.e., they forget how to use utensils). Patients may be hungry but forget how to get the food into their mouths. Most nursing homes serve food in plastic compartmentalized containers that are unfamiliar to elders who ate vegetables from a plate at home. Gastrointestinal disease can be difficult to diagnose in dementia patients.

Denture problems can cause malnutrition. Dentures began to misfit from bone resorption and in patients with substantial weight loss.   Amnestic patients frequently misplace dentures and arrive in the dining hall unable to eat. Patients with oral disease such as tooth abscess may be unable to explain symptoms and simply stop eating. Oral pharyngeal disease such as ulcers, thrush or carcinoma can also lead to weight loss and remain unrecognized because of the patient’s inability to communicate.

Secondary to poor communication, moderately demented patients may have unrecognized esophagitis, ulcer disease, diverticulitis or other gastrointestinal problems. The incidence of ulcer disease, esophagitis and other stress related gastro-intestinal problems is unclear in dementia patients. Patient’s food preferences change as the dementia progresses and “old favorites” no longer appeal to patients. Many patients desire specific types of food such as sweets, etc. Middle stage patients may neglect part of their tray because of hemi- neglect.Visually impaired patients may not see the food and hearing impaired patients may not hear instructions on eating.

Patients may receive medications such as theophyline that lower appetite. Anxious, hyperactive, frail elderly patients need adequate hydration to avoid thirst, maintain health, avoid rectal impaction and assure comfort. Aggressive hydration of all patients is essential to appropriate behavior management and patients should take about 2,000cc or 2 quarts of fluid per day unless the patient is fluid restricted or has congestive heart failure.

Dehydration is common in dementia patients and contributes to behavioral problems. Although active hydration increases incontinence, well hydrated patients are more comfortable and easier to manage.

End Stage

End stage dementia patients lose weight for many reasons. Feeding apraxia is common (i.e., the patient forgets how to chew or swallow). These patients are still able to bite. The mechanical ability of severely demented patients is similar to that of a small child who has not learned to eat solids. Patients with end stage dementia lose the drive to eat and recognition of food as sustenance. Feeding apraxia occurs slowly in severely demented patients. The abrupt onset of refusal to eat is more likely secondary to stroke, depression or some mechanical problem. The gastrointestinal tract continues to function in dementia despite the inability to consume food substances.   End stage patients are at risk for aspiration (i.e., inhaling food or mechanical obstruction of upper airway).

Management Strategies

Dementia patients should eat with glasses, dentures and hearing aids intact with batteries. Patients with visual impairment should have the food placed within their field of attention.   Patients with feeding apraxia should be prompted or fed. Patients with swallowing apraxia should be given food consistencies that they can tolerate. Medical problems such as peptic ulcer disease, chronic constipation or rectal impaction can be medically treated to lessen patient discomfort and increase appetite. Hallucinations, delusions and depression can be treated with appropriate doses of psychotropic medications. Patients unable to sit for more than 15 minutes for a meal can be given frequent snacks between meals as hunger is a common reason for agitation in patients.

End stage patients require feeding tubes or G-tubes to maintain body mass. Patients unable to swallow, eat or care for themselves have permanent severe neurological damage and will not regain cognitive function. The decision of whether to prolong suffering in an otherwise severely brain-damaged patient is a difficult, ethical consideration.   The decision requires the input of family, pastor and other responsible individuals. Hospice care is appropriate for Alzheimer’s patients and individuals dying with dementia should be treated like those with cancer or other terminal medical problems.


Copyright © 2008


Promising Alzheimer’s Treatment Being Tested by Neuro Company and U.S. Research University

(NeuroEM Therapeutics) A Phoenix-based medical device R&D company, announced today that it has begun a study with a premiere research university (University of South Florida) to test its Transcranial Electromagnetic Treatment (TEMT) in aged primates.

“All attempts to treat Alzheimer’s through drugs have thus far been very disappointing, so our medical device represents a new therapeutic direction,” said Dr. Gary Arendash, President and CEO of NeuroEM Therapeutics.

“Aged primates (Rhesus monkeys) develop the same abnormal amyloid deposits in their brains as Alzheimer’s patients and they also become cognitively impaired during aging,” Dr. Arendash indicated.

He and his colleagues had previously found that their patent-pending TEMT technology reverses both Alzheimer’s brain pathology and severe memory impairment in aged Alzheimer’s mice.  These mice had been genetically modified to produce human amyloid deposits, which are thought to cause Alzheimer’s disease.

However, primates are much closer to humans in brain structure and function.  Moreover, they spontaneously develop amyloid plaques in their brains during aging identical to those in human AD patients.  A therapeutic that is found to be beneficial to these aged primates is likely to provide the same benefits in Alzheimer’s patients.

For the study, researchers at NeuroEM’s collaborating university are administering TEMT to aged primates over several months while monitoring cognitive performance and brain function.  TEMT is completely non-invasive, so subjects will not even be aware of it.

“The primates being used in this study are all substantially aged, which affords us a unique opportunity to get important, Alzheimer’s-related data during the treatment period,” stated Dr. Arendash.  Dr. Chuanhai Cao at the University of South Florida, who helped develop TEMT technology with Dr. Arendash, is performing the study’s biochemical analyses.

TEMT has two ways that it directly attacks the Alzheimer’s disease process.  First, it disaggregates amyloid plaques both inside and outside of brain cells.  Secondly, it increases brain metabolism by enhancing mitochondrial function.  Both of these mechanisms are unique to TEMT in that no drug being clinical tested against Alzheimer’s offers them.

“If our collaborative primate study is successful, clinical trials with TEMT administration to Alzheimer’s patients could begin by next summer,” indicated Dr. Arendash.  “NeuroEM Therapeutics has a projected time line to commercialize its medical device of under 5 years, which is much faster than for an Alzheimer’s drug,” said Dr. Arendash.

NeuroEM’s head device for Alzheimer’s treatment is designed to be self-contained for comfortable in-home treatment, allowing complete mobility.  The company has several pending patents for use of TEMT against neurodegenerative diseases.  Numerous studies have shown the technology to be safe for humans.  The head device would only be available through neurologists and other health professions qualified to diagnose Alzheimer’s Disease.

Alzheimer’s affects over 5 million Americans, with the U.S. market being $4-10 billion annually for an effective therapeutic. More information about NeuroEM Therapeutics and TEMT technology can be found at the company’s website (


© NeuroEM Therapeutics, Inc., 2014


Hello Brain: Online Resource Encourages Everyone to Improve Brain Health

(Medical News Today) An innovative website promoting brain health has been launched in Trinity College Dublin as part of a new EU Commission initiative to increase the societal impact of brain research.

More people across the EU are now living longer than ever before. However failing mental function can frequently impair the quality of those extra years. The Hello Brain campaign brings together the latest information on brain health together with the latest brain research in a bid to raise public awareness of the importance of investing in brain health in order to support independent living in our older years.

The diversity of cognitive functioning observed in older adults, together with the scientific discovery that the brain is plastic, has sparked considerable European research seeking ways to maintain cognitive function, prevent decline, extend independent living and promote active and healthy ageing. The campaign hopes to help the general public understand how their brain works, what science is discovering about that remarkable mass of fatty tissue inside our head and how to keep it healthy.

The Hello Brain campaign, which is the public face of the ASAPS project (A Sharing Approach to Promoting Science), received €1 million funding from the EU Commission under its Seventh Framework Programme.

The project, led by Trinity College Dublin, is co-ordinated by Dr Sabina Brennan, Principal Investigator at the Institute of Neuroscience and Assistant Director of Trinity’s NEIL (Neuro-Enhancement for Independent Lives) Programme. Significantly, the campaign translates complex scientific information into is easy-to-understand, practical health and well-being information designed to encourage people to be more proactive about their brain health so that they can live independently for longer.

The Hello Brain website, (available in English, French and German) provides practical tips on how to keep your brain healthy using a range of entertaining videos and online resources, including the Hello Brain Health App which can be downloaded for free.

The Hello Brain App provides daily suggestions to support brain health and it is available for smartphone (iPhone and Android) as well as iPad. The campaign has also developed a web-version of the App for those who prefer to work from their computer and a hardcopy version, available to download from the website, for those who prefer pen and paper.

The campaign invites users to take the Hello Brain Challenge “to do one thing every day that’s good for your brain health”. Social media platforms Facebook and Twitter help to make the campaign more interactive, encouraging a sense of community participation among users.

Hello Brain website includes six short animations (all approx. 2 minutes) specifically produced for the campaign:

  • What will your life look like in 50 years?
  • Will I lose my memory when I get old?
  • How can I keep my brain sharp when my body gets old?
  • Is exercise good for my brain?
  • Is it ever too late to follow your childhood dreams?
  • What makes your brain work?

There are also six video interviews in which international scientists discuss topical issues in brain health and research

  • Can my leisure activities protect my cognitive function?
  • Can I change my brain?
  • What is neuroplasticity and why is it important?
  • The Upsides of ageing
  • Retirement, memory and usefulness
  • Challenge, Change and Learning

And an hour length documentary, entitled The Age of The Brain.

Speaking about the background for the campaign, Dr Brennan, commented:

“We asked people across Europe what they feared most about growing old and they told us that they feared losing their memory and losing their independence. They also told us that dementia was the disease that they feared most.”

“However what most people don’t know is that research is showing that ‘modifiable’ lifestyle factors like physical and mental exercise and social engagement can help to protect brain health and function. We want to make the general public aware of this so that they can benefit from this scientific knowledge and be more proactive about their own brain health.”

“Your brain is one of the most complex systems we know of in the Universe, and as with all living things the environment affects how it works. For your brain, that environment is how you live, how physically active you are, how much you engage with other people, how you sleep and eat and whether you occupy your brain with tasks that can strengthen it.”

According to Professor Brian Lawlor, Conolly Norman Professor of Old Age Psychiatry at Trinity and Consultant Psychiatrist at St James’s Hospital,

“The scientific evidence is starting to show that our lifestyle can have a major impact on how our brains function and react to the ageing process. Being physically active, building positive connections with the people around us, challenging our brain, and managing our diet, diabetes, hypertension and stress are all linked with better brain health.”

However, the Hello Brain campaign is not just aimed at older populations but is something everyone needs to think about.

“Even young adults in their mid-20s could benefit and should consider protecting their brains now for the future,” added Professor Lawlor. “Think of it like a pension fund. Healthy brain habits now build the brain’s cognitive reserve for later on. It’s a lodgement, an investment in your ‘brain bank’ for later in life.”

There are currently 150 million people aged over 50 in Europe and one of the primary ways that they use the Internet is to educate themselves about their health. The Hello Brain campaign and website capitalise on the growth of digital literacy among European citizens in order to share important and relevant scientific information about ageing in a way that will educate and empower, whilst also addressing the digital divide by providing some campaign material s in more traditional formats.

Highlighting the significance of the website for GPs, Professor Lawlor said:

“Many of your patients may feel that memory loss and dementia are inevitable parts of ageing. Hello Brain can help you make them aware that this is not necessarily the case, and to illustrate the steps that they can take now to potentially protect their brain and memory in the longer term.”


Source: Trinity College Dublin

© 2004-2014 All rights reserved.


Scientists Create New ‘Designer Proteins’ in Fight Against Alzheimer’s and Cancer

(University of Leicester) Chemists at the University of Leicester have reported a breakthrough in techniques to develop new drugs in the fight against diseases such as cancer and Alzheimer’s.

The team has developed an innovative process allowing them to generate a particular type of synthetic amino acid – and a particular type of designer protein – that has not been done before.

The advance is announced by the Jamieson Research Group in the Department of Chemistry at the University of Leicester.  Their work, funded by the Engineering and Physical Sciences Research Council (EPSRC), is published in the Royal Society of Chemistry journal Organic and Biomolecular Chemistry.

Dr Andrew Jamieson, lead scientist, said:

“We are very proud of this research, it has taken several years of hard work to master the chemistry techniques to create these new building blocks but now that we have conquered it we have access to new building blocks that people have only ever dreamed of before!”

Amino acids are Mother Nature’s building blocks. They are used to make all proteins and so are essential for life, however Mother Nature only uses twenty of these building blocks. The Leicester research involves the chemical synthesis of unnatural amino acids that can be used to make unnatural mini-proteins with new 3D structures and importantly new functions.

Dr Jamieson said:

“We are particular interested in using our new building blocks to develop innovative new protein drugs for the treatment of cancer and Alzheimer’s disease.

“Unnatural amino acids, the building blocks, are described as chiral, meaning they have “handedness”. A robust synthesis to selectively produce molecules with a particular handedness has not previously been reported.

“Our new practical method allows us to selectively synthesise only the “right handed molecules”.

“This new research is important because it has uncovered a new, easier and quicker way to make these building blocks which can be used to make new drugs.  We now have access to new building blocks to develop innovative new protein drugs for the treatment of disease.

“We are actively using these building blocks to develop new treatments for cancer and Alzheimer’s disease. We have also had a summer student use the building blocks to synthesise a toxin produced by a sea snail, and hope to develop this as a new pain killer.”

Dr Jamieson said innovative new strategies are required for drug discovery that can provide highly potent drugs with no side-effects. Access to these new building blocks is the first step in developing their innovative new protein drug strategy.


  • Robust Asymmetric Synthesis of Unnatural Alkenyl Amino Acids for Conformationally Constrained a-Helix Peptides
  • Organic & Biomolecular Chemistry, 2014, DOI: 10.1039/C4OB01832J
  • Download the Accepted Manuscript PDF

Copyright – The University of Leicester Website, as a database, is eligible for protection under copyright and Database Right. These rights are owned by the University of Leicester.


Memory Slips in Senior Years and Dementia Risk

(WebMD) Healthy elderly people who begin reporting memory lapses are significantly more likely to be diagnosed with dementia roughly a decade later, new research suggests.

Evaluating more than 500 seniors, scientists found that those with memory complaints were almost three times more likely to develop mild cognitive impairment (memory and thinking problems) — a potential precursor to Alzheimer’s disease — within nine years. Additionally, 80 percent had full-blown dementia within a dozen years.

“I would say if you’re an elderly person and you’re noticing serious changes in your memory, you should take it seriously, but it’s certainly not a cause for immediate alarm,” said study author Richard Kryscio, associate director of University of Kentucky’s Sanders-Brown Center on Aging.

“If you’re a middle-aged person, I would sort of ignore this,” he added. “The average age of the people we started [the study] with was 73… and nothing happened until they were in their 80s, so there’s plenty of time.”

The study is published in the Sept. 24 online edition of the journal Neurology.

Alzheimer’s disease is the most common type of dementia. It causes profound memory loss that is also characterized by impairments in language, focus, judgment and visual perception, according to the Alzheimer’s Association. About 5.2 million Americans have been diagnosed with Alzheimer’s, which is progressive, incurable and eventually leads to death.

The study participants were asked annually about any noticeable changes in their memory, and took memory and thinking tests, for an average of 10 years. After death, 243 participants’ brains were examined for evidence of Alzheimer’s disease during autopsies.

Among other results, nearly 56 percent of participants reported memory lapses overall, at an average age of 82. People carrying a gene increasing the risk of Alzheimer’s had double the odds of experiencing brain impairment. Smokers complaining of memory problems took less time to transition to mild cognitive impairment, the findings showed.

Kryscio said he was mildly surprised to see how many years it took for dementia to set in among those experiencing earlier memory lapses. This extended period potentially offers time to prevent further problems from developing, he noted, but no proven dementia interventions currently exist.

Dr. Anton Porsteinsson, director of the Alzheimer’s Disease Care, Research and Education Program at University of Rochester School of Medicine in New York, called the study “well thought-out.” He said its focus mirrors that of much other research in the field.

Despite the lack of proven dementia interventions, Porsteinsson said, certain lifestyle changes can help memory, including quality sleep, exercise, a healthy diet and brain-stimulating activities.

“Those are things that are reasonable to initiate, especially in those getting worried or noticing some changes in their memory,” he said.

“The challenge here, in terms of interventions, is that there is no single thing that offers a solution,” Porsteinsson added. ”

But for now, for people who do feel their memory is changing in a consistent or significant way, it makes sense for them to at least bring this up with their health care provider and consider whether some changes in lifestyle can contribute to healthy cognitive aging.”


By Maureen Salamon
Copyright © 2013-2014 HealthDay. All rights reserved.


Self-reported Memory Complaints

Neurology. 2014 Sep 24. pii: 10.1212/WNL.0000000000000856. [Epub ahead of print]

Self-reported memory: Implications from a longitudinal cohort with autopsies.

Kryscio RJ1, Abner EL2, Cooper GE2, Fardo DW2, Jicha GA2, Nelson PT2, Smith CD2, Van Eldik LJ2, Wan L2, Schmitt FA2.

Author information



We assessed salience of subjective memory complaints (SMCs) by older individuals as a predictor of subsequent cognitive impairment while accounting for risk factors and eventual neuropathologies.


Subjects (n = 531) enrolled while cognitively intact at the University of Kentucky were asked annually if they perceived changes in memory since their last visit. A multistate model estimated when transition to impairment occurred while adjusting for intervening death. Risk factors affecting the timing and probability of an impairment were identified. The association between SMCs and Alzheimer-type neuropathology was assessed from autopsies (n = 243).


SMCs were reported by more than half (55.7%) of the cohort, and were associated with increased risk of impairment (unadjusted odds ratio = 2.8, p < 0.0001). Mild cognitive impairment (dementia) occurred 9.2 (12.1) years after SMC. Multistate modeling showed that SMC reporters with an APOE ε4 allele had double the odds of impairment (adjusted odds ratio = 2.2, p = 0.036). SMC smokers took less time to transition to mild cognitive impairment, while SMC hormone-replaced women took longer to transition directly to dementia. Among participants (n = 176) who died without a diagnosed clinical impairment, SMCs were associated with elevated neuritic amyloid plaques in the neocortex and medial temporal lobe.


SMC reporters are at a higher risk of future cognitive impairment and have higher levels of Alzheimer-type brain pathology even when impairment does not occur. As potential harbingers of future cognitive decline, physicians should query and monitor SMCs from their older patients.


© 2014 American Academy of Neurology.


Turmeric Compound Boosts Regeneration of Brain Stem Cells

(BioMed Central) bioactive compound found in turmeric promotes stem cell proliferation and differentiation in the brain, reveals new research published today in the open access journal Stem Cell Research & Therapy. The findings suggest aromatic turmerone could be a future drug candidate for treating neurological disorders, such as stroke and Alzheimer’s disease.

The study looked at the effects of aromatic (ar-) turmerone on endogenous neutral stem cells (NSC), which are stem cells found within adult brains. NSC differentiate into neurons, and play an important role in self-repair and recovery of brain function in neurodegenerative diseases. Previous studies of ar-turmerone have shown that the compound can block activation of microglia cells. When activated, these cells cause neuroinflammation, which is associated with different neurological disorders. However, ar-turmerone’s impact on the brain’s capacity to self-repair was unknown.

Researchers from the Institute of Neuroscience and Medicine in Jülich, Germany, studied the effects of ar-turmerone on NSC proliferation and differentiation both in vitro and in vivo. Rat fetal NSC were cultured and grown in six different concentrations of ar-turmerone over a 72 hour period. At certain concentrations, ar-turmerone was shown to increase NSC proliferation by up to 80%, without having any impact on cell death. The cell differentiation process also accelerated in ar-turmerone-treated cells compared to untreated control cells.

To test the effects of ar-turmerone on NSC in vivo, the researchers injected adult rats with ar-turmerone. Using PET imaging and a tracer to detect proliferating cells, they found that the subventricular zone (SVZ) was wider, and the hippocampus expanded, in the brains of rats injected with ar-turmerone than in control animals. The SVZ and hippocampus are the two sites in adult mammalian brains where neurogenesis, the growth of neurons, is known to occur.

Lead author of the study, Adele Rueger, said:

“While several substances have been described to promote stem cell proliferation in the brain, fewer drugs additionally promote the differentiation of stem cells into neurons, which constitutes a major goal in regenerative medicine. Our findings on aromatic turmerone take us one step closer to achieving this goal.”

Ar-turmerone is the lesser-studied of two major bioactive compounds found in turmeric. The other compound is curcumin, which is well known for its anti-inflammatory and neuroprotective properties.

Journal Reference:

  1. Joerg Hucklenbroich, Rebecca Klein, Bernd Neumaier, Rudolf Graf, Gereon Fink, Michael Schroeter, Maria Rueger. Aromatic-turmerone induces neural stem cell proliferation in vitro and in vivo. Stem Cell Research & Therapy, 2014; 5 (4): 100 DOI: 10.1186/scrt500

Copyright ©2014 by AAAS, the science society.