Saturday, 25 April 2009

23 MAY '09 (Saturday) Talk on “INTRODUCTION ON EXERCISE” by Physiotherapist, Ms Tracy Chan.

Dear Members,

ADFM KL-PJ Alzheimer’s Caregivers Support Group Committee, in conjunction with its support group monthly gathering, has arranged a Talk “INTRODUCTION ON EXERCISE” by Physiotherapist, Ms Tracy Chan.

The Committee welcome all Members and the Public to this Talk.

Details of the Talk:

TIME: 2:30 PM
VENUE: ADFM Taman Seputeh Day Care Centre, 9A, Lorong Bukit Raja, Taman Seputeh, 58000 Kuala Lumpur


The aim of this session is to provide the older/geriatric population of society information on the benefits of exercise, especially for people with dementia and for the prevention of dementia.

The benefits of exercise have been recognized by all in the medical and para medical professions. These benefits range from reduced risks/incidences of various diseases like colon, breast, prostate and rectal cancers, type 2 Diabetes Mellitus, coronary artery disease, osteoporotic fractures and falls to improvements in cardio vascular functions, lipid profiles, mental functions etc.. It also has been shown to reduce the risk of developing dementia, delay the onset of dementia and slow down its progression.

There are different types of exercise for different purposes. Exercise could be vigorous, moderate or light. There are aerobic exercises as well as strengthening exercises. In order to avoid injury, it is recommended that one undergoes warming up before any exercise and cooling down after the exercise.

Although exercise is good for most of the older / geriatric population, precautions have to be taken by those having heart problems, uncontrolled metabolic disease, and uncontrolled hypertension for example and those with chronic problems like joint replacements, stroke, heart surgery arthritis and chronic obstructive pulmonary disease.


This session on Exercise is presented by MsTracy Chan, a physiotherapist. Tracy obtained her Bachelor of Allied Health Sciences (Physiotherapy) from the University of Sydney, her Graduate Certificate in Orthopaedic Manual Therapy from Curtin University and her Graduate Diploma in Neurological Rehabilitation from the University of Western Australia. She has worked in various private hospitals for 5 years and thereafter on her own and for various NGO’s.


kindly confirm your attendance to:

ADFM Secretariat, Katherine Leong /Janet Low at Tel: 603 – 7956 2008 / 7958 3008 OR Email to:

OR you can register online with the ADFM National Alzheimer's Caregivers Online Network (NACON) at:

Welcome you to join our National Alzheimer's Caregivers Online Network (NACON) if you are not a Member yet. To join, click at:

From: KL-PJ Alzheimer's Caregivers Support Group Committee &
National Alzheimer's Caregivers Online Network (NACON)

Friday, 24 April 2009


Anti-inflammatory pain relievers such as Ibupofren (Advil, Motril) and naproxen (Aleve) may delay the onset of Alzheimer's but do not prevent it, according to a new medical study.

Earlier studies indicated that such nonsteroidal anti-inflammatory drugs (NSAIDs), which include aspirin, could protect against Alzheimer's, a degenerative disease linked to inflammation in the brain.

The new research, published in the April 22 online issue of Neurology, the Jurnal of the American Academy of Neurology, has shown the opposite effect, with NSAIDs increasing the risk of Alzheimer's by 66 percent.

The study involved 2,736 subjects with an average age of 75 who did not suffer dementia when enrolled. Followed over a period of 12 years, the group included 351 heavy users of ibuprofen or naproxen prior to enrollment, and 107 who became heavy users during the study.

At the end of the research, 476 patients had developed Alzheimer's or some form of dementia.

Researchers determined that heavy NSAIDs users had 66 percent greater chance of developing Alzheimer's or dementia than those with little or no NSAID use.

"A key difference between this study and most of those done earlier is that our participants were older," said study author John Breitner, of the Department of Veterans Affairs and the University of Washington in Seattle.

"It has been argued for some time that NSAID use delays the onset of Alzheimer's disease. It would follow that studies looking at younger people who use NSAIDs would show fewer cases of Alzheimer's, while in groups of older people there might be more cases, including those that would have occurred earlier if they had not been delayed," he added.

"This is one interpretation of the results, but other explanations are possible," Breitner cautioned, adding that further research was needed to understand why NSAIDs increased the risk of dementia.

Characterized by forgetfulness, agitation and dementia, Alzheimer's is caused by a massive loss of cells in several regions of the brain, driven by a buildup of plaques of amyloid protein. The disease occurs most frequently in old age.

An estimated 37 million people worldwide, including 5.3 million in the United States, live with dementia, with Alzheimer's disease causing the majority of cases, according to the World Health Organization (WHO).

With the aging of populations, this figure is projected to increase rapidly over the next 20 years.

(Source: AFP, 22 April 2009)

Thursday, 23 April 2009


Older diabetics whose blood sugar drops to dangerously low levels have a higher risk of developing dementia, latest study from U.S. Researchers.

The study by Researchers at Kaiser Permanente in Oakland, California, suggests that aggressive blood sugar control resulting in blood sugar so low it requires a trip to the hospital may increase dementia risks in older adults with type 2 diabetes.

"We know that having blood sugar that is too high is not good," said Rachel Whitmer, a Kaiser research scientist whose study appears in the Journal of the American Medical Association.

"You want to keep that blood sugar at a good level, but you don't want to go too low," she said.

Several studies have found that diabetics have a higher risk of developing Alzheimer's disease. The most common form of dementia - than do the general population. And others have shown that diabetics who take insulin and pills to help control their disease have a lower Alzheimer's risk.

The very current issue here is balance of blood sugar control.

A number of things such as a missed meal can cause severe low blood sugar in diabetics, but the chief cause is too much insulin, which can happen in people who take insulin injections or with oral diabetes drugs such as sulfanylureas or glimepiride that cause the body to make more insulin.

The research study looked at more that two decades of data in more than 16,600 patients with type 2 diabetes.

The Research Team checked to see if prior episodes of low blood sugar that were severe enough to require a trip to the hospital were associated with a higher risk of dementia.

They found that compared with people who had no severe bouts of low blood sugar, diabetics with single or multiple episodes had higher dementia risks, and risk levels rose depending on the number of severe hypoglycemic episodes.

The study said in older patients with a history of one episode, they had a 26 percent greater risk of dementia. Patients with two episodes had a 115 percent greater risk of dementia. And patients with three or more episodes had a 160 percent greater risk of dementia.

The study offers more evidence that aggressive measures to control blood sugar can cause harm in elderly diabetics.

It follows three recent trials that found tight glycemic control could cause heart disease and death in some elderly diabetics.

The Research Team plan to look at dementia risks for people in the study who took glitazones - a class of drugs that help diabetics use insulin better. Drugs in this class include GlaxoSmithKline's Avandia or rosiglitazone and Takeda Pharmaceutical's Actos or pioglitazone.

Alzheimer's is the most common form of dementia among older people, affecting 5.2 million people in the United States, according to the Alzheimer's Association. Some 23.6 million Americans have diabetes, according to the American Diabetes Association.

(Source: Reuters, 14 April 2009)

Tuesday, 21 April 2009


Dear All,

ADFM KL-PJ AD Caregivers Support Group Committee, in conjunction with our monthly gathering, is organizing a talk on:

TIME: 2:30 PM

Registration begins at 2:00pm


Alzheimer's disease is a neurological disease that typically affects older adults from the age of 65 onwards. The causes for this disease can be multi-factorial, meaning it can be due to many different factors including genetics and environmental influence. It is known that there are some genes which are thought to give you a risk factor for developing AD in later life.

AD can also be inherited and usually these family members develop AD at a much earlier age (before 50 years of age). In these families, there is a strong genetic component and some of the genes have been identified.

Current research into AD is focused on trying to understand the influence of genes in the development of the disease, and how we can interfere with the progression of the disease.

This talk will try to explain the current research into AD and what it means for the future treatment of this devastating disorder.


Dr Azlina is a Lecturer at the University Malaya. She is also doing some research on the brain, and is interested in how memory works.

Dr Azlina used to be involved with the KL-PJ AD Support Group between the years 1999-2000 before she left for her PhD in UK. She always had fond memory of the loving, fighting spirit of the caregivers as they face this disease with their loved ones.


Kindly confirm your attendance to:

ADFM Secretariat, Kath Leong /Janet Low at Tel: 603 – 7956 2008 / 7958 3008 OR Email to:

OR you can register online with the ADFM National Alzheimer's Caregivers Online Network (NACON) at:

Welcome you to join our National Alzheimer's Caregivers Online Network (NACON) if you are not a Member yet. To join, click at:

From: KL-PJ Alzheimer's Caregivers Support Group Committee &
National Alzheimer's Caregivers Online Network (NACON)

Sunday, 19 April 2009


Older adults who worry about their health often opt out of physical activity and as a result, they may have greater trouble walking and getting around as they age, new research suggests.

A key component to avoid walking difficulty in older adults is to resolve health worry issues earlier in life, the Researchers from the Department of Nutrition and Exercise Science at Oregon State University in Corvallis suggest in the current issue of Research Quarterly for Exercise and Sport, where their research is published.

Some studies have suggested that “health worry” may motivate people to exercise regularly and engage in other healthy behaviors. The current study, however, suggests that’s not always the case.

Among a representative sample of 7,527 adults aged 70 and older participating in the Longitudinal Study of Aging, people with a high degree of health worry engaged in less physical activity than those who worried less about their health.

Furthermore, people who participated in less physical activity were more likely than their more active counterparts to report having trouble walking 6 years later.

Because physical function decreases with age and safety concerns arise, older adults may not choose physical activity as a response to health worry.

They also note that health professionals, the media, fitness instructors and family and friends may use warnings of illness or premature death to try to motivate aging couch potatoes to exercise or at least become more physically active. However, the current study suggests that this may be counterproductive; aging adults may become so fearful of their health that they will avoid physical activity.

Study shows using threats and fear-tactics to encourage physical activity in older adults will not work.

The current study suggests a more productive approach in dealing with health concerns in the aging population is to provide health-related information and screening tools prior to beginning a physical activity routine to help cope with health worries. This might ease health concerns and promote participation in physical activity.

The simple message from this study is that people should be encouraged to walk. To encourage walking, people should avoid fear-raising tactics. Rather, the emphasis should be on walking for fun, for health and for transportation.

The study warned that fear-inducing strategies often cause older adults to worry about things like falling and that diminishes their desire to walk, which in turn diminishes their ability to walk.

(Source: Research Quarterly for Exercise and Sport, March 2009.)

Saturday, 18 April 2009


The Alzheimer's Disease Foundation Malaysia (ADFM) Penang AD Support Group cordially invites YOU to their Public Talks on:

Date: Sunday, 3 May 2009
Time: 3.00 p.m. to 5.00 p.m.
Venue: Kompleks Masyarakat Penyayang
(Seminar Room 4, Caring Society Complex), Jalan Utama, Penang

Registration begins at 2.30 p.m.

3.00pm - Welcome Address by Mr Tan Yeow Joo, Chairman, ADFM Penang AD Support Group

3.10pm - Opening Address by Dr P Srinivas, Consultant Geriatrician and Advisor, ADFM Penang AD Support Group

3.20pm - “Dementia – Duty to CARE”
By Mr Willie Kwa, Mental Health Practitioner for the Elderly in UK

3.50pm - “Caring for the Care-Giver”
By Ms Margarita Malayapillay, President Penang Association of Counselling and Psychology

4.10pm - Questions and Answers

4.30pm - Refreshment

For reservation, kindly contact:
Tel: 604-6564537 / Fax: 6573202 or call Chairman, Mr YJ Tan at: 604-6565291 or Email:


A Community Project organized by Penang AD Support Group & supported by Novartis.


Dear All,

TIME: 2:30 PM

The KL-PJ Alzheimer's Caregivers Support Group Committee WELCOME ALL MEMBERS AND THE PUBLIC to attend the above Talk in conjunction with our monthly gathering.

Synopsis: “How To Exercise The Brain”

Do you find it difficult to remember things? Do you easily forget someone's name or often forget where you parked the car? Everyone loses their memory from time to time, it is a part of normal life.

People often want to know how to improve their memory, and one way to do this is by exercising your brain! The brain is similar to muscle- the more you use it, the stronger it gets. To improve your memory, you can focus on certain tasks to exercise the brain.

This talk will introduce the structures in the brain involved in memory and also briefly explain how the brain records the information. We'll see why people with Alzheimer's disease have a specific type of memory loss and how this impacts on their behaviour.

We will then discuss some practical ideas on how to get the most of your own memory.

Speaker's Profile: Dr Azlina Ahmad Annuar

Dr Azlina is a Lecturer at the University Malaya. She is also doing some research on the brain, and is interested in how memory works.

Dr Azlina used to be involved with the KL-PJ AD Support Group between the years 1999-2000 before she left for her PhD in UK. She always had fond memory of the loving, fighting spirit of the caregivers as they face this disease with their loved ones.


kindly confirm your attendance to:

ADFM Secretariat, Katherine Leong /Janet Low at Tel: 603 – 7956 2008 / 7958 3008 OR Email to:

OR you can register online with the ADFM National Alzheimer's Caregivers Online Network (NACON) at:

Welcome you to join our National Alzheimer's Caregivers Online Network (NACON) if you are not a Member yet. To join, click at:

From: KL-PJ Alzheimer's Caregivers Support Group Committee &
National Alzheimer's Caregivers Online Network (NACON)

Monday, 13 April 2009


Healthy older people shouldn't bother spending money on computer games and websites promising to ward off mental decline, according to the author of a review of scientific evidence for the benefits of these "Brain Exercise" Programmes.

"These marketed products don't confer any additional benefit over and above being socially and intellectually active in one's normal daily life," said Dr Peter J. Snyder of Lifespan Affiliated Hospitals in Rhode Island in the United States.

"There are somethings that we could be doing that have much more rigorous data to support their application."

Types of "Brain Training" are known to help people with memory problems function better, but their benefit for those who don't have measurable cognitive impairment isn't clear, Synder and his Team noted.

Meanwhile in an interview, Synder said the market for these products has swelled from US$2 million (RM) in 2005 to an estimated US$225 million this year.

To review evidence on the benefits of cognitive training for healthy older people, Snyder and his colleagues analyzed 10 randomized controlled trials of a variety of approaches, ranging from a popular computer-based programme to individualized piano lessons.

While there was some evidence that brain training helped people's immediate performance on tasks related to the training, there was no evidence that the effects could be generalized to other areas of mental function. Further, just half of the studies included extended follow-up, so evidence for long term benefits was slim.

The findings don't mean that brain training isn't helpful for people who have memory problems, nor are they definitive proof that brain exercise can't help keep healthy people's wits sharp.

But social and intellectual engagement in day-to-day life, from reading to grandchildren to doing crossword puzzles, is "probably just as effective or more effective" than any formal brain exercise programme, he said. Further, these activities are free.

Also, there is strong scientific evidence that being physically active every day preserves cognitive function. Because cardiovascular disease and Type 2 diabetes are both known to contribute to mental decline, exercising and taking other steps to maintain heart health and a healthy weight will help keep the brain healthy too.

(Source: NST, 12 April 2009 from Reuters)


Higher levels of aluminum in drinking water appear to increase people's risk of developing Alzheimer's disease, whereas higher levels of silica appear to decrease the risk, according to French investigators.

"Alzheimer's is a multifactorial disease, and aluminum concentrations in drinking water may have an effect on cognitive decline and Alzheimer's," said Dr Virginie Rondeau.

The results of some studies suggest that silica reduces the oral absorption of aluminum or increases the excretion of this metal.

Rondeau, at the Institute National de la Sante et de la Recherche Medicale in Bordeaux, and her colleagues examined associations between exposure to aluminum or silica from drinking water and the risk of cognitive decline, dementia, and Alzheimer's among elderly subjects followed for 15 years.

Daily aluminum intake of at least 0.1 milligramme was associated with greater cognitive decline during the course of the study.

Subjects with a high daily aluminum intake had a 2.26-fold increased risk of dementia, the Researchers noted. On the other hand, for every 10 milligramme per-day intake of silica, the odds of developing dementia dropped by 11 percent.

(Source: NST, 12 April 2009 from Reuters)

Sunday, 12 April 2009


You've heard that diabetes hurts your heart, your eyes, your kidneys. New research indicates a more ominous link: That diabetes increases the risk of getting Alzheimer's disease and may speed dementia once it strikes.

Doctors long suspected diabetes damaged blood vessels that supply the brain. It now seems even more insidious, that the damage may start before someone is diagnosed with full-blown diabetes, back when the body is gradually losing its ability to regulate blood sugar.

In fact, the lines are blurring between what specialists call "vascular dementia" and scarier classic Alzheimer's disease. Whatever it's labeled, there's reason enough to safeguard your brain by fighting diabetes and heart-related risks.

"Right now we can't do much about the Alzheimer's disease pathology," those sticky plaques that clog patients' brains, says Dr. Yaakov Stern, an Alzheimer's specialist at Columbia University Medical Center. But, "if you could control these vascular conditions, you might slow the course of the disease."

The link has staggering societal implications: More than 5 million Americans have Alzheimer's, and cases already are projected to skyrocket in the next two decades as the population ages. The question is how much the simultaneous obesity-fueled epidemic of Type 2 diabetes may worsen that toll.

There are about 18 million Type 2 diabetics who are considered to have at least two to three times a non-diabetic's risk of developing Alzheimer's. Still, Type 2 diabetes often leads to heart disease and other conditions that kill before Alzheimer's typically strikes, in the 70s.

Don't panic if you're diabetic, stresses Dr. Ralph Nixon of New York University, vice chairman of the Alzheimer's Association's scientific advisory council. Genetics still are the prime risk factor for dementia.

"It by no means means that you're going to develop Alzheimer's disease, and certainly many people with Alzheimer's don't have diabetes," he cautions.

But the latest research strengthens the link, and has scientists asking if diabetes and its related "metabolic syndrome" increase risk solely by spurring brain changes that underlie Alzheimer's - or if they add an extra layer of injury to an already struggling brain, what Nixon calls "essentially a two-hit situation."

Among the findings:

Brain functioning subtly slows as Type 2 diabetics' blood-sugar rises, well before people have any obvious memory problems.

In a major national study, doctors gave a battery of cognitive tests to nearly 3,000 diabetics. Every 1 percentage point increase in their A1C score — an average of glucose control over a few months — meant small but meaningful drops in memory, the ability to multitask, and other cognitive tasks, Wake Forest University scientists wrote last month in the journal Diabetes Care.

The government-funded study is testing whether better treatment to lower those A1C scores in turn improves brain function.

At Columbia, Stern is co-directing a powerful study: Hundreds of aging New York City residents agreed to regular testing while they were still healthy, allowing scientists to catch the earliest signs of dementia. Stern tracked yearly changes in 156 who developed Alzheimer's, and found that those who had a history of diabetes and high cholesterol worsened faster, he reports this month in a special issue of Archives of Neurology dedicated to the link.

Type 2 diabetes occurs as a result of insulin resistance, as the body gradually loses sensitivity to this hormone that's essential for turning blood sugar into energy. A similar effect in the brain helps explain the dementia link, Dr. Suzanne Craft of the Veterans Affairs Puget Sound Health Care System concludes in a research review also published in that journal. Insulin influences memory in a variety of ways, and an insulin-resistant body in turn affects brain cells' insulin-related activity.

Other factors such as brain inflammation and cell-damaging oxidative stress may play a role, too. But clearly more affected is a silent dysfunction of glucose control, not something that suddenly begins after diabetes is diagnosed.

"You want to think of it more as a continuum than just whether or not you have diabetes," Stern says.

While scientists sort out exactly what's going on, the research does point to some common-sense protections: If you have diabetes, closely follow your doctor's advice for controlling it. Try to lower high cholesterol and blood pressure that can harm the brain's blood supply and exacerbate memory problems.

And if you're still healthy, Nixon advises "hedging your bets against Alzheimer's" with the same steps that help prevent both diabetes and heart disease - A Good Diet and Plenty of Exercise.

(Source: AP, 17 March 2009)


A gene known to raise the risk of Alzheimer's disease may alter brain activity throughout life, British Researchers reported recently.

They found that young adults with the so-called APOE4 gene type had distinct brain patterns and their finding might lead to a better test for Alzheimer's risk.

Even when they were not doing anything, people with the APOE4 gene had busier brains than people with other forms of the APOE gene, the Researchers reported in the Proceedings of the National Academy of Sciences.

When they did a Memory Task, the APOE4 carriers had more activity in a part of the brain called the hippocampus, which is involved in long-term memory and navigation and which is the first area known to be affected in Alzheimer's disease.

It could be that the brain just wears itself out in some people, said Dr. Christian Beckmann of Imperial College London, who worked on the study.

"We were surprised to see that even when the volunteers carrying APOE4 weren't being asked to do anything, you could see the memory part of the brain working harder than it was in the other volunteers," Beckmann said in a statement.

"Not all APOE4 carriers go on to develop Alzheimer's, but it would make sense if in some people, the memory part of the brain effectively becomes exhausted from overwork and this contributes to the disease."

The APOE4 gene variant is found in about a quarter of the population. Not everyone who has it develops Alzheimer's but those who have one copy have four times the normal risk and people with two copies have 10 times the risk.

"These are exciting first steps toward a tantalizing prospect: a simple test that will be able to distinguish who will go on to develop Alzheimer's," Dr. Clare Mackay of the University of Oxford, who led the study, said in a statement.

The Researchers used a type of real-time imaging called functional magnetic resonance imaging or fMRI to look at the brains of 36 volunteers aged 20 to 35, 18 who had at least one copy of APOE4.

None of the volunteers had any memory problems and the Researchers stressed the findings did not mean they were fated to develop Alzheimer's.

"We have shown that brain activity is different in people with this version of the gene decades before any memory problems might develop," Mackay said.

"We've also shown that this form of MRI, where people just lie in the scanner doing nothing, is sensitive enough to pick up these changes."

Dr. Peter Nestor of the University of Cambridge, a Neuroscientist who was not involved in the study, said more research is clearly needed.

"The findings of this study are of considerable interest but should not be over-interpreted to mean that Alzheimer's disease is already starting to develop in this young, healthy group of volunteers," Nestor said in a statement.

(Source: Reuters, 06 April 2009)


A dysfunction in protein folding contributes to nerve cell death in Alzheimer's disease, a finding that could help lead to new treatments, Dutch researchers report.

The presence of tangles of misfolded proteins is believed to contribute to Alzheimer's disease, the experts explained. A process known as the "unfolded protein response" typically protects cells from the toxic effects of accumulated misfolded proteins. But prolonged activation of the unfolded protein response such as that seen in Alzheimer's patients may result in cell death.

The researchers at the VU University Medical Center in Amsterdam and the University of Amsterdam believed that unfolded protein response contributed to brain damage through its effects on the accumulation of hyperphosphorylated tau, a major component of tangles in the brains of people with Alzheimer's.

The study revealed that markers of the unfolded protein response were expressed in areas of tau accumulation in Alzheimer's patients. The unfolded protein response-related proteins were expressed early, in pre-tangle neurons, but were absent in tangle neurons.

The findings suggest that "unfolded protein response activation occurs at an early stage of neurofibrillary degeneration and ... that the prolonged activation of the [unfolded protein response] is involved in both tau phosphorylation and neurodegeneration in [Alzheimer's disease] pathogenesis ... Future studies will address the therapeutic opportunities of this pathway for the treatment of [Alzheimer's disease] and other tauopathies," the Researchers wrote.

(Source: HealthDay, 02 April 2009 - The American Journal of Pathology, April 2009 Issue.)


A simple Balance Test may help doctors predict a decline in memory and brain function in people with Alzheimer's Disease, research shows.

In a study, Researchers found that Alzheimer's patients with an abnormal One-Leg Balance Test experienced greater decline in brain function over 2 years than those with a normal One-Leg Balance Test.

"Our results reinforce, in an Alzheimer's Disease population, the growing evidence suggesting a link between physical performances and cognitive decline," Study Chief Dr. Yves Rolland, of the University of Toulouse III, France, noted in a written statement.

"If these results are confirmed by other data, the One-Leg Balance Test could be adopted in clinical practice to identify Alzheimer's Disease patients at high risk of rapid cognitive decline," the Researcher added.

According to a report of the study published in the Journal of Alzheimer's Disease, 686 patients with Alzheimer's Disease were evaluated by a Geriatrician every six months for up to two years, and their degree of cognitive impairment was measured.

At the same time, a "One-Leg Balance" Test was given, where a participant was asked to stand on one leg for as long as possible. The test was considered abnormal when the participant was unable to stand on one leg for 5 seconds or more.

At the outset, roughly 15 percent of the study subjects had an abnormal One-Leg Balance Test and these patients were significantly older and had significantly more severe cognitive impairment.

In analysis taking into account factors that might influence the results, the Researchers found that subjects with an abnormal One-Leg Balance Test had significantly greater decline in memory and thinking at 12, 18, and 24 months.

For example, the average decline on the Mini-Mental State Examination at 24 months was 9.2 points when balance impairment was present, compared with just 3.8 points with no balance impairment.

"The One-Leg Balance Test is a Stress Test that may characterize subjects with low cognitive reserve," Rolland and colleagues concluded.

(Source: Reuter, 31 March 2009 - Extract from Journal of Alzheimer's Disease, March 2009.)


People who have a high family risk of developing depression had less brain matter on the right side of their brains on par with losses seen in Alzheimer's disease, U.S. Researchers reported recently.

Brain scans showed a 28-percent thinning in the right cortex -- the outer layer of the brain -- in people who had a family history of depression compared with people who did not.

"The difference was so great that at first we almost didn't believe it. But we checked and re-checked all of our data, and we looked for all possible alternative explanations, and still the difference was there," said Dr. Bradley Peterson of Columbia University Medical Center and the New York State Psychiatric Institute.

The study appears in the Proceedings of the National Academy of Sciences.

The findings are based on imaging studies of 131 people aged 6 to 54 with and without a family history of depression.

The team was looking specifically for abnormalities in the brain that could signal a predisposition to depression, rather than changes that may be caused by the disease.

The thinning on the right side was only linked with a family predisposition to depression. People who actually were depressed also had thinning on the left side of cortex.

"Because previous biological studies only focused on a relatively small number of individuals who already suffered from depression, their findings were unable to tease out whether those differences represented the causes of depressive illness, or a consequence," Dr Bradley Peterson said.

Having a thinner right cortex may increase the risk of depression by disrupting a person's ability to decode and remember social and emotional cues from other people.

They did memory and attention tests on the study subjects and found the less brain material a person had in the right cortex, the worse they performed on attention and memory tests.

The findings suggest rather strongly that if you have thinning in the right hemisphere of the brain, you may be predisposed to depression and may also have some cognitive and inattention issues.

Dr Bradley Peterson said the findings suggest medications used to treat attention problems such as stimulants might be useful in the treatment of depression in some patients.

(Source: Reuters, 23 March 2009)


It's known that people who suffer a brain injury have a higher-than-normal risk of developing Alzheimer's disease, and now lab experiments suggest a reason why.

Alzheimer's disease is associated with accumulations of an abnormal protein, amyloid beta, in the brain. Traumatic brain injury triggers accumulation of enzymes required for production of amyloid-beta, Researchers from Georgetown University Medical Center in Washington, DC, report in the Research Journal Nature Medicine.

"Past research has shown that traumatic brain injury is a risk factor for developing Alzheimer's Disease (AD) in later life," Dr. Mark P. Burns explained to Reuters Health. Many autopsies of brains of people who suffered a traumatic brain injury "have amyloid deposits similar to those seen in Alzheimer's."

Research shown that a biochemical pathway that is active long-term in AD is activated short term in the days immediately following traumatic brain injury.

Burns and his colleagues found that blocking the enzymes in this pathway reduced the effects of brain injury in mice. "We found we could dramatically reduce the amount of brain damage that occurred," he said. "This led to a large reduction in physical disability, and a reversal of the learning problems that occurred after brain injury."

"As there is currently no treatment for traumatic brain injury," Burns concluded, "our research identifies new targets for drug therapy."

Furthermore, the drugs that inhibit the enzymes involved in amyloid beta production "are currently under evaluation in AD clinical trials, so could be quickly made available for traumatic brain injury clinical trials."

(Source: Reuters, 27 March 2009)