Elderly With Low Vitamin B12 Risk Brain Shrinkage And Cognitive Decline

Elderly individuals with low blood vitamin B12 levels have a greater risk of brain shrinkage and losing their cognitive skills, researchers from Rush University Medical Center, Chicago reported in the journal Neurology. Foods rich in vitamin B12 are mainly from animals and include, eggs, milk, liver, meat, and fish.

Christine C. Tangney, Ph.D. and team carried out a study with 121 individuals aged at least 65 years from the south side of Chicago. They underwent blood tests to check for their levels of B12 and B12-related metabolites which can give an indication of a B12 deficiency. They were also assessed for memory and other cognitive skills. About four-and-a-half years later magnetic resonance imaging (MRI) scans of their brains were taken to see how big their brains were, as well as identifying some other signs of brain damage.

Those with four of five markers for vitamin B12 deficiency were found to have a higher risk of getting lower cognitive test scores and smaller total brain volumes.

Christine C. Tangney said:

“Our findings definitely deserve further examination. It’s too early to say whether increasing vitamin B12 levels in older people through diet or supplements could prevent these problems, but it is an interesting question to explore. Findings from a British trial with B vitamin supplementation are also supportive of these outcomes.”

Cognitive scores ranged from -2.18 to +1.42 – the average score was 0.23. Homocysteine is a marker of B12. For every rise of one micromole per liter of homocysteine cognitive scores dropped by 0.03 points.

It was not the vitamin B12 blood level that was linked to smaller brain size or cognitive problems, Tangney explained. It was the markers that indicate B12 deficiency. Low vitamin B12 is much harder to detect in elderly individuals.

The National Institute of Aging funded the study.

Vitamin B12

Vitamin B12 or Cobalamin is a water soluble vitamin – it dissolves in water and travels through the bloodstream. It is one of eight B vitamins. The human body cannot store Vitamin B12, any excess is excreted through urine.

The molecular formula for vitamin B12 is C63H88CoN14O14P.

Cobalamin is a general term for compounds containing the dimethylbenzimidazolylcobamide nucleus of vitamin B12.

Vitamin B12 plays a key role in normal nervous system functioning and brain development. It is also involved in the formation of red blood cells.

Cobalamin plays a role in the metabolism of every cell in the human body, experts say. It affects DNA synthesis and regulation, as well as the synthesis of fatty acids and energy production.

Structurally, vitamin B12 is the most complicated of all the vitamins, as well as being the largest. Cobalamin can be industrially produced through bacterial fermentation synthesis.

Vitamin B12 is a large molecule, the most complicated of all the vitamins

Vegans should take vitamin B12 dietary supplements to avoid deficiency, because this vitamin comes from animal sourced proteins. Supplements are generally presented as cyanocobalamin, which the body easily converts to the active forms of methylcobalamin and 5-deoxyadenosylcobalamin.

Written by Christian Nordqvist

Multiple sclerosis affects around 400,000 people in the United States and 2.5 million people worldwide. While there is no cure, scientists have found a potential treatment to stop multiple sclerosis progression in its tracks in the form of the experimental drug laquinimod.
A potential oral drug may help prevent and reduce the progression of MS.

Multiple sclerosis (MS) is a disease of the central nervous system, whereby the immune system attacks tissue in the brain and spinal cord. The damage to the tissue called the myelin sheath – an insulated, fatty covering that protects the nerve fibers – affects how nerves carry electrical signals from the brain and the spinal cord.

Currently, MS treatment involves the use of prescription drugs and rehabilitation. MS is a lifelong disease with no known cure. However, the disease can be controlled using both disease-modifying and symptomatic treatments.

Disease-modifying therapies reduce the number of relapses and may help slow disease progression; symptomatic therapies contribute to relieving some of the symptoms.

The research – published online in an American Academy of Neurology medical journal Neurology: Neuroimmunology & Neuroinflammation – discovered that laquinimod might prevent the development of MS or slow down the progression of MS in mice.

“These results are promising because they provide hope for people with progressive MS, an advanced version of the disease for which there is currently no treatment,” says study author Scott Zamvil, M.D., Ph.D., of the University of California-San Francisco and a Fellow of the American Academy of Neurology.

Laquinimod is a drug in development for relapsing-remitting MS (RRMS) and primary progressive MS. RRMS is characterized by unexpected, recurring relapses. While in around 80 percent of all patients the disease begins as RRMS, most go on to develop secondary progressive MS after 10 years, which describes gradually increasing disability, without recovery periods.

The precise way in which laquinimod works is unclear. It is suggested that the drug alters the behavior of immune cells and prevents them from entering the brain and spinal cord, thus reducing damage to myelin.

Studies have indicated that laquinimod may have both an anti-inflammatory action and the capacity to protect the nerve structure and function.

For this research, Zamvil and colleagues gave mice that develop a spontaneous type of MS oral laquinimod or a placebo(water) daily. The number of T and B cells in the mice were then analyzed.

Laquinimod reduces clusters of myelin-destroying cells

T and B cells usually assist with the body developing immunity to infection. However, in MS, T and B cells help create antibodies that attack and destroy myelin.

In the first study, which included 50 mice, results showed that of the mice that were given oral laquinimod, 29 percent developed MS, compared with 58 percent of mice that received the placebo. Also noted was a 96 percent reduction in harmful clusters of B cells, which are only found in people with progressive MS. The researchers say that this evidence indicates that the drug may prevent MS.

In the second study, which included 22 mice, laquinimod was administered after mice had developed paralysis. The team observed a reduction in progression of the disease. Compared with the mice receiving the placebo, the mice that were given laquinimod presented a 49 percent decrease of dendritic cells that help create specialized T cells, a 46 percent reduction in T cells and a 60 percent drop in harmful antibodies.

“This study has given us more insight into how laquinimod works. But because this was an animal study, more research needs to be done before we know if it could have similar results in people.”

Scott Zamvil, M.D., Ph.D.

People with MS have to receive medication throughout their lifetime. Active Biotech, the manufacturer of laquinimod, points out that, a once-daily oral treatment creates a substantial advantage for patients compared with existing products on the market, all of which need to be injected.

When it comes to health in later life, researchers find laughter may really be the best medicine. A new study – led by Georgia State University – suggests combining laughter with moderate exercise may improve the mental health of older adults, as well as boost their motivation and ability to engage in physical activity.
old laughing
Adding laughter to physical activity may provide a wealth of benefits for older adults.

Lead author Celeste Greene, from the Gerontology Institute at Georgia State, and colleagues report their findings in The Gerontologist.

It is well established that physical activity at any age is beneficial for health. For older adults, regular physical activity can boost heart health, aid weight control, reduce diabetes risk, improve bone health, and maintain and grow muscle strength.

According to the Centers for Disease Control and Prevention (CDC), adults aged 65 years and older should engage in at least 150 minutes of moderate-intensity aerobic activity (such as brisk walking) or 75 minutes of vigorous-intensity aerobic activity (such as jogging) every week.

Additionally, seniors should engage in muscle-strengthening activities – such as sit-ups or simply carrying heavy bags – at least 2 days a week.

However, a recent study from the CDC found that more than 1 in 4 adults in the United States aged 50 and older – the equivalent to around 31 million Americans – do not engage in regular exercise.

‘Putting the fun in fitness’ for older adults

Greene and team note that one major barrier to regular exercise for older adults is lack of motivation, largely due to low enjoyment of physical activity.

For their study, the researchers set out to investigate whether combining laughter with physical activity would boost exercise enjoyment for older adults, enabling them to reap the associated health benefits.

“We want to help older adults have a positive experience with exercise, so we developed a physical activity program that specifically targets exercise enjoyment through laughter,” explains Greene.

“Laughter is an enjoyable activity and it carries with it so many health benefits, so we incorporated intentional laughter into this program to put the fun in fitness for older adults.”

The program the researchers created is known as LaughActive. It incorporates moderate-intensity physical activity with simulated laughter techniques, whereby participants choose to laugh, without there being any humorous stimuli.

This simulated laughter initiates eye contact and playful behaviors with other participants, the team notes, which triggers genuine laughter.

The researchers explain that the body is unable to pinpoint the difference between simulated and genuine laughter, so either form offers health benefits.

Laughter boosted motivation to exercise

The team enrolled 27 older adults to their study, all of whom were residing in assisted living facilities.

As part of the LaughActive program, the adults were required to attend two 45-minute sessions a week for 6 weeks.

These sessions included a workout routine involving strength, balance, and flexibility exercises, as well as eight to 10 laughing exercises, each lasting 30-60 seconds, which were typically performed after every two to four physical exercises.

All subjects completed questionnaires that assessed their perceived benefits of participating in the LaughActive program. Their mental health and aerobic endurance – that is, the ability to exercise for long periods without getting tired – were also assessed.

At the end of the 6-week program, 96.2 percent of participants reported laughter as an enjoyable addition to physical activity, while 88.9 percent said they felt the laughter aspect of the program helped increase exercise accessibility and made them want to continue.

Laughter boosted the motivation to take part in other exercise programs or activities for 88.9 percent of participants, the researchers report.

“The combination of laughter and exercise may influence older adults to begin exercising and to stick with the program.”

Celeste Greene

What is more, the LaughActive program was associated with significant improvements in mental health and aerobic endurance among participants.

Based on their results, Greene and colleagues believe incorporating laughter with physical activity could be a good way to improve both the mental and physical health of older adults.

Furthermore, the team says such an approach may encourage older adults with functional or cognitive impairments to reap the health benefits of laughter; they point out that simulated laughter does not require cognitive skills to “get the joke,” because there is no joke to understand.

While their study findings show promise, the researchers point out that they are early results in a small number of participants, so further studies are needed to gain a better understanding of how laughter may benefit health.

A vaccine for Alzheimer’s disease could be trialed in humans within the next 3-5 years, after researchers from the United States and Australia have uncovered a formulation that they say successfully targets brain proteins that play a role in development and progression of the disease.
syringe and vials
Researchers say the Alzheimer’s vaccine could be tested on humans within 3-5 years.

Study co-author Prof. Nikolai Petrovsky, of Flinders University School of Medicine in Australia, and colleagues reveal how a vaccine combination generates antibodies that target beta-amyloid and tau proteins in the brain – both of which are considered hallmarks of Alzheimer’s disease.

Beta-amyloid is known to accumulate in the brains of people with Alzheimer’s, forming plaques, while the tau protein forms tangles. Plaques and tangles are believed to disrupt signaling between nerve cells and contribute to nerve cell death.

“[The proteins are] a bit like the car in your driveway,” Prof. Petrovsky explained to ABC Adelaide. “You need to remove them from the brain otherwise if you left broken down cars in your driveway eventually you couldn’t get out.”

“Essentially that’s what happens in people who get Alzheimer’s or dementia is they have lots of these broken down proteins in the brain.”

Reporting in the journal Scientific Reports, the team describes how the vaccine formulation has proven safe and effective in mouse models of Alzheimer’s, and it has also successfully targeted beta-amyloid and tau proteins in human brain tissue.

Vaccine combo boosts antibody response to Alzheimer’s proteins

Researchers have spent decades searching for ways to prevent and treat Alzheimer’s, but success has been limited.

Between 2002-2012, 413 clinical trials were conducted worldwide that assessed the safety and efficacy of 244 compounds against Alzheimer’s. Only one new drug came out of these trials – representing a 0.4 percent success rate – and this drug only induces short-term relief of Alzheimer’s symptoms.

As a result of such poor outcomes from clinical trials to date, the National Institutes of Health (NIH) increased their funding for Alzheimer’s research by $350 million, bringing the total funding for research in the U.S. to $1.3 billion this year.

According to Prof. Petrovsky and colleagues, such funding has led to the development of their “exceptional” vaccine, which they say is comprised of a MultiTEP vaccine platform and Advax.

The team explains that the MultiTEP approach produces high antibody responses to beta-amyloid and tau proteins either independently or combined, while Advax is an adjuvant vaccine that further boosts the antibody response.

In their study, the researchers found that the formulation was effective and well-tolerated in Alzheimer’s mouse models, with no reports of adverse reactions. The vaccine was also able to target the proteins in brain tissue from patients with Alzheimer’s.

“This study suggests that we can immunize patients at the early stages of AD [Alzheimer’s disease], or even healthy people at risk for AD, using our anti-amyloid-beta vaccine, and, if the disease progresses, then vaccinate with another anti-tau vaccine to increase effectiveness.”

Study co-author Prof. Michael Agadjanyan, Institute for Molecular Medicine, California

According to the Alzheimer’s Association, around 5.4 million people in the U.S. are living with Alzheimer’s, and this number is expected to almost triple by 2050 unless new, effective treatment strategies are uncovered.

The researchers say they will be working with four companies to assess the non-clinical safety and toxicology of the vaccine, which is required under the U.S. Food and Drug Administration’s (FDA) Investigational New Drug program.

If the vaccine continues to show success in these preclinical trials, the researchers say they could be testing the vaccine in individuals at high risk for Alzheimer’s or those in the early stages of the disease within the next 3-5 years.

Scientists have long known that there is a strong association between diabetes and Alzheimer’s, but the nature of that relationship – and how to treat it – was unclear. Now Melissa Schilling, an innovation professor at NYU, has discovered the pathway between diabetes and Alzheimer’s, and it has big implications for how Alzheimer’s can be prevented.

Professor Schilling compared and integrated decades of research on diabetes, Alzheimer’s, and molecular chemistry, focusing in particular on results that seemed to yield conflicting results. It turns out that routine practices in research – like excluding all patients with known medical problems such as diabetes from an Alzheimer’s study, for example – had obscured the mechanisms that connect the two diseases. Those main mechanisms turn out to be insulin and the enzymes that break it down. The same enzymes that break down insulin also break down amyloid-beta, the protein that forms tangles and plaques in the brains of people with Alzheimer’s. When people have hyperinsulinemia (i.e., they secrete too much insulin due to a poor diet, pre-diabetes, early diabetes, obesity, etc.) the enzymes are too busy breaking down insulin to break down amyloid-beta, causing amyloid-beta to accumulate.

The American Diabetes Association estimates that roughly 8.1 million Americans have undiagnosed diabetes and 86 million have pre-diabetes and have no idea. The good news is that hyperinsulinemia is preventable and treatable through changes in diet, exercise, and medication. Schilling notes, “If we can raise awareness and get more people tested and treated for hyperinsulinemia, we could significantly reduce the incidence of Alzheimer’s disease, as well as other diabetes-related health problems. Everyone should be tested, early and often, preferably with the A1C test that doesn’t require fasting.Dementia patients should especially be tested – some studies have shown that treating the underlying hyperinsulinemia can slow or even reverse Alzheimer’s.”

Professor Schilling’s research has been published in Journal of Alzheimer’s Disease.

COPD – short for chronic obstructive pulmonary disease – is a chronic lung condition that is usually associated with tobacco smoking.

COPD is a collection of separate lung conditions – usually both chronicbronchitis and emphysema – which cause airflow limitation, i.e. difficulty breathing.1-4

Contents of this article:

  1. COPD facts, statistics and anatomy
  2. Causes, symptoms and diagnosis of COPD
  3. Treatments for COPD, prevention and management

Fast facts on COPD:

Here are some key points about COPD. More detail and supporting information is in the main article.

  • COPD is a group of diseases that includes chronic bronchitis and emphysema
  • Most cases of COPD are a result of tobacco smoking
  • Symptoms of COPD include shortness of breath, coughing and production of sputum
  • COPD is a progressive and incurable disease, and the third largest cause of death in the US
  • In 2010, more than 70,000 women died of COPD in the US, compared to more than 64,000 males11
  • A single symptom of COPD (such as cough, shortness of breath) often arises long before other symptoms.
  • The lungs of people with COPD suffer structural damage that causes the tiny air sacs to enlarge and become less efficient
  • Diagnosis is confirmed by a clinical test called spirometry, which measures by how much the breathing is limited
  • The main way to prevent COPD developing is to avoid smoking
  • Any patient with COPD can benefit from smoking cessation and there are medical interventions, including drugs, to help with this
  • COPD cannot be reversed but its symptoms can be eased by drug treatment
  • Drug treatments are usually inhaled, and most act as bronchodilators through muscle relaxation to ease breathing by opening up the lungs
  • Other therapy options include pulmonary rehabilitation, oxygen therapy, and surgery
  • Exacerbations and complications of COPD are an unusual worsening of symptoms and can be life-threatening. Healthcare professionals help patients to prevent complications as far as possible.

What is COPD?

COPD is irreversible and most often caused by smoking.

COPD stands for chronic obstructive pulmonary disease:

  • Chronic because it is ongoing – it persists lifelong without being fully reversible
  • Obstructive because normal breathing capacity is restricted
  • Pulmonary because it pertains to the lungs – it is a respiratory disease.

Chronic bronchitis is continual irritation and inflammation of the lining of the lungs, causing them to thicken and secrete mucus. The diagnosis is made if cough or mucus production persists for long enough.

Emphysema is damage to the structure of the lung in which the walls of the air sacs are destroyed, making the air spaces larger and less efficient.

The airflow limitation in COPD is usually progressive – it gets worse over time – and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases. The condition does not change much over the course of several months.


Leading cause of illness and death

The American Lung Association says COPD is the third-leading cause of death in the US, claiming the lives of 134,676 Americans in 2010.11

The World Health Organization (WHO) has estimated that prevalence of COPD in the US rose by 41% between 1982 and 1994, with death rates going up by 71% between 1966 and 1985. It also estimates that COPD is responsible for 4.8% of all deaths – or an estimated 2,745,816 deaths in 2002.4

In 2011, 12.7 million US adults (aged 18 and over) were estimated to have COPD, but almost 24 million adults in the US have evidence of impaired lung function, suggesting that COPD is underdiagnosed.12,13

Increasingly, women are more likely to be affected by COPD, with 2010 the eleventh year in which rates of COPD-related deaths in women have exceeded deaths in men.11 In fact, women are twice as likely as men to be diagnosed with chronic bronchitis, and more women than men are now diagnosed with emphysema (a disease that was historically more prevalent in men).

The 2011 statistics for men and women are as follows:13

  • Chronic bronchitis – 3.3 million men/6.8 million women
  • Emphysema – 2.1 million men/2.6 million women.
More than 2.3 million people across the globe are living with multiple sclerosis. At present, there is no cure for the condition. However, researchers believe they are close to uncovering one: a stem cell treatment already used for some cancers has enabled wheelchair-bound patients with multiple sclerosis to walk again.
Worldwide, more than 2.3 million people have MS.

Multiple sclerosis (MS) is a debilitating disease of the central nervous system (CNS). It is believed to be an autoimmune disease, in which the immune system mistakenly attacks the brain, spinal cord and optic nerves.

In detail, the immune system attacks myelin – the protective coating surrounding nerve fibers – as well as the nerve fibers themselves. Such damage impairs communication between the brain and spinal cord, producing a variety of symptoms.

Common symptoms of MS include numbness or tingling of the face and body, walking and balance difficulties, involuntary muscle spasms, pain, weakness, fatigue, dizziness and cognitive impairment. Some people with MS may also experience seizures, speech problems or tremors.

Relapsing-remitting MS (RRMS) is the most common form of the disease, accounting for around 85% of all cases. In RRMS, people experience flare-ups of symptoms, followed by periods of partial or complete recovery.

Secondary-progressive MS (SPMS) normally follows RRMS. This occurs when symptom flare-ups cease and the disease starts to progress more steadily.

MS: a debilitating disease with no cure

According to the National Multiple Sclerosis Society, around two thirds of people with MS retain their ability to walk, though many individuals may require the assistance of a cane or crutches to get around. In severe cases, some patients may become wheelchair-bound.