Showing posts with label Alzheimer's. Show all posts
Showing posts with label Alzheimer's. Show all posts

January 27, 2015

Tuesday, January 27, 2015
A new study reveals that higher doses or prolonged use of medications with anticholinergic effects significantly increases the risk for developing dementia.  Although, this is not the first study to discover such a link, it is the first to suggest that the risk of dementia as a result of taking such medications may not be reversible.
“An anticholinergic agent is a substance that blocks the neurotransmitter acetylcholine in the central and the peripheral nervous system. Anticholinergics inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movement of smooth muscles present in the gastrointestinal tract, urinary tract, lungs, etc.”
Anticholinergic agents are used to treat a variety of conditions such as gastrointestinal disorders, respiratory disorders, insomnia, dizziness etc.  Some of these commonly used medications include Diphenhydramine (Benadryl, Advil PM etc.), Bupropion (Zyban, Wellbutrin), Dextromethorphan (cough suppressant) and the list goes on.  In addition, some of these medications can be acquired without a prescription and can have very strong anticholinergic effects.

Moreover, many older patients, already at higher risk of developing dementia, are frequently using these types of medications.  Doctors should be taking a proactive approach and monitoring the use of these drugs, including non-prescription use.
“For instance, the most commonly used medications in the study were tricyclic antidepressants like doxepin (Sinequan), first-generation antihistamines like chlorpheniramine (Chlor-Trimeton), and antimuscarinics for bladder control like oxybutynin (Ditropan). The study estimated that people taking at least 10 mg/day of doxepin, 4 mg/day of chlorpheniramine, or 5 mg/day of oxybutynin for more than three years would be at greater risk for developing dementia.”
Consequently, the study suggests that medical professionals should seek substitutes such as citalopram (Celexa) or fluoxitene (Prozac) for depression or loratadine (Claritin) for allergies or behavioral changes for urinary incontinence.  However, if substitutes are not available, the suggestion is to prescribe the lowest dose possible, monitor its effectiveness closely and cease use if there is no real benefit to the patient.

This study differs from other research as it used more rigorous methods, longer follow-up periods and better assessment of medication use by using pharmacy records of both prescription and non-prescription use.  It is also the first of its kind to link anticholinergic medication dosages to dementia risk.  Results were obtained by tracking nearly 3,500 Group Health seniors participating in the long-running Adult Changes in Thought study (a longitudinal population-based prospective cohort study of brain aging and incident dementia in the Seattle metropolitan area), some of which have also agreed to have their brains autopsied after they die.  Stay tuned.

Quick Facts:

Dementia is a general term for a decline in mental ability severe enough to interfere with daily life.

Alzheimer's is the most common type of dementia.

While symptoms of dementia can vary greatly, at least two of the following core mental functions must be significantly impaired to be considered dementia:

Memory
Communication and language
Ability to focus and pay attention
Reasoning and judgment
Visual perception

Many dementias are progressive, meaning symptoms start out slowly and gradually get worse.
Dementia is caused by damage to brain cells, which interferes with the ability of brain cells to communicate with each other.

There is no one test to determine if someone has dementia. Doctors diagnose Alzheimer's and other types of dementia based on a careful medical history, a physical examination, laboratory tests, and the characteristic changes in thinking, day-to-day function and behavior associated with each type.

Some risk factors for dementia, such as age and genetics, cannot be changed, however some of the most active areas of research in risk reduction and prevention include cardiovascular factors, physical fitness, and diet.

The total number of new cases of dementia each year worldwide is nearly 7.7 million, implying one new case every four seconds. The number of people with dementia is expected to nearly double every 20 years, to 65.7 million in 2030 and 115.4 million in 2050.

The costs are estimated at US$ 604 billion per year at present and are set to increase even more quickly than the prevalence.

Caring for dementia patients is overwhelming for caregivers. The stresses include physical, emotional and economic pressures. Care givers require support from the health, social, financial and legal systems.

People with dementia are frequently denied the basic rights and freedoms available to others. For example, physical and chemical restraints are used extensively in aged-care facilities and acute-care settings.

Improving the awareness and understanding of dementia across all levels of society is needed to decrease discrimination and to improve the quality of life for people with dementia and their caregivers.

More research is needed to develop new and more effective treatments and to better understand the causes of dementia. Research that identifies the modifiable risk factors of dementia is still scarce.

Higher dementia risk linked to more use of common drugs
Anticholinergic
alz.org
World Health Organization

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October 22, 2013

Tuesday, October 22, 2013
According to a new study published by Johns Hopkins Bloomberg School of Public Health, sleep quality may influence the onset and progression of Alzheimer's disease. Lead author, Adam Spira, PhD, and his team of researchers discovered a link between shorter and/or poor sleep quality and higher levels of Amyloid beta build-up in the brain.
“Amyloid beta is a peptide of 36–43 amino acids that is processed from the amyloid precursor protein (APP). While best known as a component of amyloid plaques in association with Alzheimer's disease, as Aβ is the main component of certain deposits found in the brains of patients with Alzheimer's disease, evidence has been found that Aβ is a highly multifunctional peptide with significant non-pathological activity.” 
Researchers observed self-reported sleep habits and β-Amyloid deposits of adults from the neuro-imaging sub-study of the Baltimore Longitudinal Study of Aging where the average participant age was 76 years. Subjects reported sleep that ranged from more than 7 hours to no more than 5 hours. Using the Pittsburgh compound B tracer and PET scans of the brain to determine the amount of β-Amyloid in the brain, researchers noted that shorter sleep duration and lower sleep quality were both associated with greater amounts of β-Amyloid deposits.

Even though no causal link has been established, if sleep habits do in fact have such an impact, researchers suggest that these findings could potentially slow the progression of Alzheimer’s simply by promoting and maintaining healthy sleep patterns. Furthermore, as this is not the first study to link sleep and Alzheimer’s disease, more research with objective sleep measures could determine whether poor sleep actually contributes to or accelerates Alzheimer's disease.

“Results could have significant public health implications as Alzheimer's disease is the most common cause of dementia, and approximately half of older adults have insomnia symptoms."

Alzheimer's disease is a type of dementia that causes problems with memory, thinking and behaviour. It is most common in people over 65 years of age; however up to 5% of people develop early-onset in their 40s or 50s. The most common early symptom of Alzheimer's is difficulty remembering newly learned information as changes in the part of the brain associated with learning is often the first to be affected. Eventually these individuals will experience symptoms, including disorientation, mood and behaviour changes; more serious confusion about events, time and place; unfounded suspicions about family, friends and professional caregivers; more severe memory loss and behaviour changes; followed by difficulty speaking, swallowing and walking.

Shorter Sleep Duration, Poorer Sleep Quality Linked to Alzheimer ’s Disease
Beta amyloid
Alz.org

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January 19, 2013

Saturday, January 19, 2013

Research shows that the use of choline supplements during pregnancy may prevent schizophrenia.  Specifically, lower rates of physiological schizophrenic risk factors in infants 33 days old has been noted when the dietary supplement is given during the second and third trimesters of pregnancy and early infancy.

Robert Freedman, MD, professor and chairman of the Department of Psychiatry, University of Colorado School of Medicine and one of the study's authors states: "Basic research indicates that choline supplementation during pregnancy facilitates cognitive functioning in offspring. Our finding that it ameliorates some of the pathophysiology associated with risk for schizophrenia now requires longer-term follow-up to assess whether it decreases risk for the later development of illness as well."

Choline is a water-soluble essential nutrient, typically grouped within the B-complex vitamins. It can be found naturally in foods such as liver, muscle meats, fish, nuts and eggs.  According to the American Institute of Medicine, pregnant women require between 450 and 3500 milligrams of choline each day and 550 to 3500 milligrams while lactating.  Infants aged 0-6 months need a minimum daily dose of 125 milligrams of choline and 150 milligrams from 7-12 months of age.

“Choline is also being studied for potential benefits in liver disease, including chronic hepatitis and cirrhosis, depression, memory loss, Alzheimer's disease and dementia, and certain types of seizures.”

To test their theory, researchers observed infant responses to a clicking sound.  Typically, the brain responds fully to an initial click, however the response to a second click immediately following the first is inhibited.  This trait is often absent among schizophrenia patients and relates to poor sensory filtering and familial transmission of schizophrenia risk.  Researchers observed this effect among infants to represent the illness as schizophrenia does not normally appear until adolescence.

“Half the healthy pregnant women in this study took 3,600 milligrams of phosphatidylcholine each morning and 2,700 milligrams each evening; the other half took placebo. After delivery, their infants received 100 milligrams of phosphatidylcholine per day or placebo. Eighty-six percent of infants exposed to pre- and postnatal choline supplementation, compared to 43% of unexposed infants, inhibited the response to repeated sounds, as measured with EEG sensors placed on the baby's head during sleep.”

These results could not only assist in early detection of schizophrenia, but may even help in preventing the illness or developing more effective treatments.

Some examples of choline found in different food sources:

Type of Food
mg of choline
5 ounces (142 g) raw beef liver
473
Large hardboiled egg
113
Half a pound (227 g) cod fish
190
Half a pound of chicken
150
Quart of milk, 1% fat
173
A gram soy lecithin
30
100 grams of Soybeans dry
116
A pound (454 grams) of cauliflower
177
A pound of spinach
113
A cup of wheat germ
202
Two cups (0.47 liters) firm tofu
142
Two cups of cooked kidney beans
108
A cup of uncooked quinoa
119
A cup of uncooked amaranth
135
A grapefruit
19
Three cups (710 cc) cooked brown rice
54
A cup (146 g) of peanuts
77
A cup (143 g) of almonds
74

Choline Supplementation DuringPregnancy Presents a New Approach to Schizophrenia Prevention
Choline

November 26, 2012

Monday, November 26, 2012
Researchers at the University of Texas Medical Branch at Galveston revealed that an FDA-approved medication called rosiglitazone that is used to treat insulin resistance in diabetics also enhances learning and memory. This discovery could improve cognitive performance for those with Alzheimer’s disease.

By studying genetically engineered mice designed to serve as models for Alzheimer's, “the scientists believe that the drug produced the response by reducing the negative influence of Alzheimer's on the behavior of a key brain-signaling molecule.”

The molecule in question is called extracellular signal-regulated kinase (ERK). In the brains of Alzheimer's patients as well as the mice in the study, this molecule becomes hyperactive, which leads to improper synaptic transmission between neurons thereby interfering with learning and memory.

“Rosiglitazone brings ERK back into line by activating what's known as the peroxisome proliferator-activated receptor gamma (PPARγ) pathway, which interacts with genes that respond to both PPARγ and ERK.”

Basically, the medication helps to restore signals between neurons so that cognitive functions become more normal. This research opens a gateway allowing researchers to test more FDA-approved drugs to try and normalize insulin resistance in Alzheimer's patients while potentially improving their memory at the same time. It could also lead to a greater understanding of the biology behind the cognitive issues in Alzheimer's disease.

Alzheimer's disease (AD) is the most common form of dementia. There is no cure for the disease, which worsens as it progresses, and eventually leads to death.

Symptoms:
  • Memory loss that disrupts daily life.
  • Challenges in planning or solving problems.
  • Difficulty completing familiar tasks at home, at work or at leisure.
  • Confusion with time or place.
  • Trouble understanding visual images and spatial relationships.
  • New problems with words in speaking or writing.
  • Misplacing things and losing the ability to retrace steps.
  • Decreased or poor judgment.
  • Withdrawal from work or social activities.
  • Changes in mood and personality.
Prevalence:
  • An estimated 5.4 million Americans of all ages have Alzheimer’s disease in 2012. This figure includes 5.2 million people age 65 and older and 200,000 individuals under age 65 who have younger-onset Alzheimer’s.
  • One in eight people age 65 and older (13 percent) has Alzheimer’s disease.
  • Nearly half of people age 85 and older (45 percent) have Alzheimer’s disease.
  • Of those with Alzheimer’s disease…
    • an estimated 4 percent are under age 65
    • 6 percent are 65 to 74
    • 44 percent are 75 to 84
    • 46 percent are 85 or older
  • Every 68 seconds, someone in America develops Alzheimer’s.
  • By mid-century, someone in America will develop the disease every 33 seconds.
Diabetes Drug Improves Memory, Study Suggests
Alzheimer's disease
Facts and Figures facts and figures

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October 5, 2012

Friday, October 05, 2012
Researchers from the Department of Dental Medicine and the Aging Research Center (ARC) at Karolinska Institutet and from Karlstad University in Sweden suggest that the loss of chewing ability may be linked to cognitive decline and a higher risk of dementia.

Dementia is a serious loss of global cognitive ability in a previously unimpaired person, beyond what might be expected from normal aging. It is not considered a single disease, but rather a set of signs and symptoms, in which affected areas of cognition may be memory, attention, language, and problem solving.

The study randomly selected a nationwide sample of 577 participants aged 77 or older to investigate tooth loss, chewing ability and cognitive function. Results showed that individuals that experienced more difficulty chewing hard foods were more at risk of developing cognitive impairments, even when controlling other variables such as sex, age, education and mental health. In addition, chewing with dentures or real teeth had no impact on their results.

It could be that “few or no teeth makes chewing difficult, which leads to a reduction in the blood flow to the brain. However, to date there has been no direct investigation into the significance of chewing ability in a national representative sample of elderly people.”

Unfortunately, this study does not specify whether all participants consumed similarly nutritious meals. Those with a reduced ability to chew certain foods may have been malnourished, which could have played a major role in their cognitive decline.

Nevertheless, the preliminary results of such research certainly provide further support for the fact that oral health impacts overall health. Good oral health brings significant benefits to self-esteem, dignity, social integration and general nutrition.

According the World Health Organization, the proportion of people aged 60 years and older is growing faster than any other age group, as a result of both longer life expectancy and declining fertility rates. Therefore, as our society ages, this type of research becomes more and more relevant…

  • As of 2010, more than 35.6 million people worldwide are living with dementia, or more than the total population of Canada.

  • The global prevalence of dementia stands to double every 20 years, to 65.7 million in 2030, and 115.4 million in 2050.

  • Total health-care costs for people with dementia amount to more than 1 per cent of the global gross domestic product (GDP), or US$604 billion in 2010.
Chewing Ability Linked to Reduced Dementia Risk
Dementia
Ageing
Facts about dementia

© www.mentalhealthblog.com

August 12, 2012

Sunday, August 12, 2012

William Hu, MD, PhD, assistant professor of neurology at Emory University School of Medicine and collaborators at the University of Pennsylvania and Washington University, St. Louis are getting closer to uncovering an in inexpensive and very convenient test for Alzheimer's disease. 

This type of test has been studied for several years; however reliability of results and an inability to replicate the same results have prevented such a test from being discovered.  Now, scientists have finally found a group of markers that hold up in statistical analyses in three independent groups of patients.

Basically, they measured the levels of 190 proteins in the blood of 600 participants. The subjects studied included healthy volunteers and individuals that had been diagnosed with Alzheimer's disease or mild cognitive impairment (MCI).
“A subset of the 190 protein levels (17) were significantly different in people with MCI or Alzheimer's. When those markers were checked against data from 566 people participating in the multicenter Alzheimer's Disease Neuroimaging Initiative, only four markers remained: apolipoprotein E, B-type natriuretic peptide, C-reactive protein and pancreatic polypeptide.”
Coincidentally, they discovered a correlation among patients that showed changes in their levels of these four proteins and their measurements of proteins [beta-amyloid] levels in their cerebrospinal fluid, a protein previously connected with Alzheimer's disease.  These correlations allowed researchers to group together people with MCI that may be at high risk of developing Alzheimer's.
 "We were looking for a sensitive signal," says Hu. "MCI has been hypothesized to be an early phase of AD, and sensitive markers that capture the physiological changes in both MCI and AD would be most helpful clinically." 
"The specificity of this panel still needs to be determined, since only a small number of patients with non-AD dementias were included," Hu says. "In addition, the differing proportions of patients with MCI in each group make it more difficult to identify MCI- or AD-specific changes."
Unfortunately, researchers have not yet been able to uncover a simple blood test to detect Alzheimer’s disease; however they have discovered ways to ensure that any future tests will be reliable. 

Therefore, neurologists will have to continue to diagnose Alzheimer's disease based mainly from an analysis of clinical symptoms or at times expensive PET brain imaging or painful spinal tap.

Blood Test for Alzheimer's Gaining Ground

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March 27, 2011

Sunday, March 27, 2011

According to researchers at Temple University's School of Medicine, the popular asthma drug, Zileuton, has shown potential in treating Alzheimer’s disease. This medication works by reducing the amount of amyloid beta that develops and accumulates in the aging brain. Amyloid beta is a peptide that has been known to be involved in the development of Alzheimer's disease.
“In previous studies, the Temple researchers discovered that 5-lipoxygenase, an enzyme long known to exist in the brain, controls the activation state of gamma secretase, another enzyme that is necessary and responsible for the final production of amyloid beta. When produced in excess, amyloid beta causes neuronal death and forms plaques in the brain. The amount of these amyloid plaques in the brain is used as a measurement of the severity of Alzheimer's.”
“Zileuton (trade name ZYFLO) is an orally active inhibitor of 5-lipoxygenase, and thus inhibits leukotrienes (LTB4, LTC4, LTD4, and LTE4) formation.“

Domenico Praticò and fellow researchers tested the effects of this drug on genetically engineered mice with Alzheimer's disease. Results showed that amyloid production and build-up in the brain was reduced by 50% by treating the mice with Zileuton.

Researchers are already aware of substances that can block gamma secretase’s production of amyloid, however completely eliminating a vital function may result in other health problems, such as developing cancer. “Unlike classical gamma secretase inhibitors, Zileuton only modulates the protein expression levels, which keeps some of its vital functions in tact while blocking many of its bad effects, which in this case is the development of the amyloid plaques.”

Fortunately, if clinic trials effectively demonstrate Zileuton’s ability to treat Alzheimer’s disease, the medication could be readily available to patients as it is already FDA-approved and on the market.

In addition, further research may uncover treatments for other untreatable diseases resulting from amyloid plaques accumulating in the brain, such as cerebral amyloid angiopathy, a neurological condition that occurs when amyloid proteins build up on the walls of the arteries in the brain, which increases the risk of hemorrhagic stroke and dementia.

Asthma Drug Could Help Control or Treat Alzheimer's Disease
Zileuton
Cerebral amyloid angiopathy

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August 8, 2010

Sunday, August 08, 2010
Researchers in Toronto, Canada have developed an experimental brain surgery that may delay the progression of Alzheimer’s disease. Six subjects with Alzheimer’s disease and an average age of 61 experienced this surgery called deep brain stimulation. The subjects continued to take their Alzheimer’s medication throughout the study.

Scientists implanted “electrodes in the brain's hippocampus, which plays a role in long-term memory. The electrical conductor acts as a pacemaker-like device in the head just beneath the skin. It is connected to a battery pack in the chest.”

Consequently, the mini-mental state exam, a cognitive test, revealed that half of the participants experienced a slow-down in the degenerative effects Alzheimer’s disease has on the brain, while the other half continued to decline in a manner typical of the disease’s progression.

While this new research has produced some promising results, deep brain stimulation is not a novel idea since it has been around for decades. For instance, Dr. Andres Lozano, a neurosurgeon at Toronto's University Health Network, experimented with its effects on Parkinson’s disease without success, unfortunately.

Although not all subjects experienced positive outcomes with this surgery, 64 year old, former city counselor from Brampton, Ontario, Robert Linton, recalled vivid memories of a day he spent fishing.
"I'm with my son," Linton recalled to reporters at Toronto Western Hospital. "I could see that muskie coming right at me as I was sitting in the chair, in Technicolor". "That's the power of touching a spot in your brain. I'm sold on it."
Currently, Lozano and his research team are recruiting roughly 50 people willing to install the stimulator. The plan is to activate half of the stimulators immediately and the other half only six months later all the while participants’ knowledge of its activation will remain unknown in order to truly test the benefits of the device.

Although, the true value of this device is not yet known, the actual retail cost if this treatment became available, would be between $15,000 and $20,000 per patient with a battery life of up to five years.

At the moment, I’m unsure whether I approve of this type of treatment. For one, results are insufficient therefore there is no real proof that the surgery will benefit enough people. Secondly, I am reminded of electroconvulsive therapy and I cannot get the image of Nurse Ratched delivering shock therapy out of my head…

Deep brain stimulation tested for Alzheimer's

© www.mentalhealthblog.com

January 3, 2010

Sunday, January 03, 2010
A recent study, Ginkgo Evaluation of Memory (GEM), by Beth E. Snitz, Ph.D., of the University of Pittsburgh, demonstrates that the use of the herbal supplement Ginkgo biloba does not slow the rate of cognitive decline among older adults as construed.

“The randomized, double-blind, placebo-controlled clinical trial included 3,069 community-dwelling participants, ages 72 to 96 years, who received a twice-daily dose of 120-mg extract of G biloba (n = 1,545) or identical-appearing placebo (n = 1,524). The study was conducted at six academic medical centers in the United States between 2000 and 2008, with a median (midpoint) follow-up of 6.1 years. Change in cognition was assessed by various tests and measures.”

In 2000, older adults that had normal to mild cognitive impairment were chosen and observed. The researchers placed the subjects into 3 distinct groups. Some were given a placebo over the 8 year period. Others were given either Ginkgo biloba or the placebo, where their group identity was not disclosed to the participant or the experimenter. The third group was randomly assigned to either of the groups. Double-blind studies are said to achieve greater scientific rigor than other types of research. The conclusion of this double-blind study is that Ginkgo biloba is not effective in reducing the incidence of Alzheimer dementia or dementia in general. In addition, no evidence was found to support any effects on memory, language, attention, visuospatial abilities and executive functions. Furthermore, no differences were detected through age, sex, race, education or baseline cognitive status.

Basically, no evidence was found to support the widely marketed fact that Ginkgo biloba slows the rate of cognitive decline.

What is Ginkgo Biloba?

Ginkgos are very large trees, normally reaching a height of 66–115 feet, with some specimens in China being over 50 m. The tree has an angular crown and long, somewhat erratic branches, and is usually deep rooted and resistant to wind and snow damage. A combination of resistance to disease, insect-resistant wood and the ability to form aerial roots and sprouts makes ginkgos long-lived, with some specimens claimed to be more than 2,500 years old. Extreme examples of the Ginkgo's tenacity may be seen in Hiroshima, Japan, where six trees growing between 1–2 km from the 1945 atom bomb explosion were among the few living things in the area to survive the blast. While almost all other plants and animals in the area were destroyed, the ginkgos, though charred, survived and were soon healthy again. The trees are alive to this day.

Extracts of Ginkgo leaves contain flavonoid glycosides and terpenoids and have been used pharmaceutically. Ginkgo supplements are usually taken in the range of 40–200 mg per day. Ginkgo has many alleged nootropic properties, and is mainly used as a memory and concentration enhancer, and an anti-vertigo agent. According to some studies, in a few cases, Ginkgo can significantly improve attention in healthy individuals. Allegedly, the effect is almost immediate and reaches its peak in 2.5 hours after intake.

Ginkgo has been used for…

  • Alzheimer's disease
  • Improving blood flow
  • Protecting against oxidative cell damage
  • Blocking the effects of platelet-activating factor (platelet aggregation, blood clotting)
  • Intermittent claudication
  • Easing the symptoms of tinnitus
  • Improving cognition and fatigue in those with multiple sclerosis
  • Arresting the development of vitiligo
Ginkgo may have undesirable effects, especially for individuals with blood circulation disorders and those taking anticoagulants such as ibuprofen, aspirin, or warfarin. Ginkgo should also not be used by people who are taking certain types of antidepressants (monoamine oxidase inhibitors and selective serotonin reuptake inhibitors) or by pregnant women, without first consulting a doctor.

Side effects can include…

  • possible increased risk of bleeding
  • gastrointestinal discomfort
  • nausea
  • vomiting
  • diarrhea
  • headaches
  • dizziness
  • heart palpitations
  • restlessness
Other precautions…

Ginkgo biloba leaves contain long-chain alkylphenols together with the extremely potent allergens, the urushiols (similar to poison ivy). Individuals with a history of strong allergic reactions to poison ivy, mangoes, and other urushiol-producing plants are more likely to experience an adverse reaction when consuming Ginkgo-containing pills, combinations, or extracts.

The nut-like gametophytes inside the seeds are particularly esteemed in Asia, and are a traditional Chinese food. When eaten by children, in large quantities (over 5 seeds a day), or over a long period, the raw gametophyte (meat) of the seed can cause poisoning by MPN (4-methoxypyridoxine).

Bottom line...

It is very important to remember that herbal supplements are not regulated by the FDA in the US and Canada’s regulation of such health products is quite often confusing and inconsistent. Therefore, personal responsibility is essential when relying on this type of treatment.

Ginkgo Biloba Does Not Appear to Slow Rate of Cognitive Decline

Wikipedia

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May 31, 2009

Sunday, May 31, 2009
The Lighting Research Center (LRC) has designed a pair of goggles that deliver blue light directly into the eyes. This new device is said to improve the quality of sleep for older adults. Many elderly suffer from serious sleep disturbances often times as a result of changes to their circadian rhythm. In brief, the circadian rhythm refers to the body’s 24 hour sleep/wake cycle, which relates to one’s exposure to light and shifts in hormone levels.

Many recent studies over the past few years have demonstrated the effectiveness of blue light in stimulating the circadian system. All types of light travel through the retina to the circadian clock in the brain. Unfortunately, several changes to the eyes and brain as well as lifestyle adjustments come with age, which can seriously impact the amount of light stimulus reaching the retina, therefore affecting the circadian clock. In addition, our lenses thicken and our pupils shrink with age, hence further reducing the amount of light that can pass through the retina.

Furthermore, the elderly may suffer from mental health conditions, such as Alzheimer’s disease, that require even more light to keep the circadian rhythm in tact because of weaker neural connections in the brain. Less time spent outdoors also reduces the amount of daylight taken in preventing a good night’s sleep.

“The device was worn by eleven subjects between the ages of 51 and 80 years of age. Each subject was exposed to two levels of blue light (about 50 lux and 10 lux) from the personal light-treatment device for 90 minutes on two separate nights. Blood and saliva samples were collected at prescribed times to assess levels of nocturnal melatonin, a hormone used as a marker for the circadian clock, with high levels at night when a person is in a dark environment and low levels during the day."

The light-induced nocturnal melatonin was suppressed by about 35% with low levels of light exposure and about 60 percent with high levels of light after only one hour of wearing the glasses. Nocturnal melatonin appeared to be more rapidly suppressed and sustained with higher levels of blue light.

The study provides hope that a practical, comfortable, and effective solution may soon be available for those suffering from circadian sleep disorders.

Light-treatment Device To Improve Sleep Quality In The Elderly

© www.mentalhealthblog.com

January 26, 2009

Monday, January 26, 2009
The US Food and Drug Administration gave the green light to Geron to commence the world’s first clinical trial involving human embryonic stem cells. “By early summer, a handful of patients with severe spinal cord injuries will be eligible for injections of specialized nerve cells designed to enable electrical signals to travel between the brain and the rest of the body.”

During the initial phase of this trial, safety of the treatment will be assessed, before moving on to the potential discovery of a variety of therapeutic benefits. Prior benefits have already been revealed among rats who regained their ability to control their hind legs as a result of stem cell injections.

To begin with, what are embryonic stem cells?
These stem cells come from embryos that are four to five days old. At this stage, an embryo is called a blastocyst and has about 150 cells. These are pluripotent (ploo-RIP-uh-tunt) stem cells, meaning they can divide into more stem cells or they can specialize and become any type of body cell. Because of this versatility, embryonic stem cells have the highest potential for use to regenerate or repair diseased tissue and organs in people.

Clearly, “anti-abortion groups have opposed the trial, and the Society for the Unborn Child even called the proposal ‘sick’. A spokesperson for the organization claimed that, “It involves cannibalising an unborn child”.

Many might claim that destroying human life in hopes of saving human life is unethical; however the benefits well outweigh the costs. For instance, stem cell research could potentially assist in the treatment of a wide range of medical problems such as Parkinson’s disease, Alzheimer’s disease, heart disease, stroke, diabetes (Type 1), birth defects, replacement or repair of damaged organs, and reduce risk of transplantation. Moreover, even if diseases are not cured, this research could lead to a more improved quality of life for many people. "I would absolutely love to see a quadriplegic regain use of their thumb," said UC Irvine neuroscientist Hans Keirstead.

Although controversial, would it not be reasonable to admit that we should work toward sustaining healthy lives with stem cell research as long as abortion remains legal?

Stem cell therapy to be tested on spinal cord injuries

New Stroke Research Trial Stirs More Controversy Over Stem Cells

Stem cells: What they are and what they do

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November 29, 2008

Saturday, November 29, 2008
The Swedish medical university Karolinska Institutet (KI) published a doctoral thesis that links Alzheimer’s disease with high levels of fast food intake. In the study, Susanne Akterin observed mice that were fed diets rich in fat, sugar and cholesterol. After only nine months, the rats had developed what looked like the preliminary stages Alzheimer’s disease. More specifically, the irregularities found in the brain had greatly resembled those of early Alzheimer’s.

Although the exact causes of Alzheimer’s disease remains unknown, there are many identified risk factors, such as “a variant of a certain gene that governs the production of apolipoprotein E, one of the functions of which is to transport cholesterol”. This study sought to demonstrate the link between this risk factor and diet in mice.

Basically, the brains of these rats were modified to mimic the effects of the apoE4 gene variant by ingesting a diet similar to fast food for nine months. The results showed a chemical change in the brain comparable to that found in Alzheimer’s patients.
The change in question was an increase in phosphate groups attached to tau, a substance that forms the neurofibrillary tangles observed in Alzheimer’s patients. These tangles prevent the cells from functioning normally, which eventually leads to their death. Ms Akterin and her team also noted indications that cholesterol in food reduced levels of another brain substance, Arc, a protein involved in memory storage.

In short, the results of this study suggest that a diet high in fat/cholesterol combined with genetics can potentially contribute to the development of Alzheimer’s disease. Although, there has been no direct causal link identified, the study has provided yet another reason to lay off the burgers and fries.

Fast Food A Potential Risk Factor For Alzheimer’s

© www.mentalhealthblog.com

April 20, 2008

Sunday, April 20, 2008

Researchers of the Layton Aging & Alzheimer's Disease Center at Oregon Health and Science University (OHSU) in Portland have discovered that brain volume is linked to mental decline in people with Alzheimer's.

This linkage was discovered while performing autopsies on deceased elderly patients. The entire brain was found to be larger in patients who had not experienced any cognitive impairment. In particular, the hippocampus, a part of the forebrain in the medial temporal lobe that plays a major role in long term memory, has been discovered to be larger in size for those patients with no cognitive impairments. Most surprising, those in both categories had plaques and tangles in the brain as found in typical Alzheimer patients.

The study consisted of 12 patients who did not have Alzheimer's symptoms before death and 24 who had experienced symptoms of the disease. As per Dr. Deniz Erten-Lyons, the brains of those without symptoms of Alzheimer’s were found to be on average 10% larger.

Dr Jeffrey Kaye, director of the Layton Aging and Alzheimer's Disease Center and a professor of neurology in the OHSU School of Medicine stated: "We are hopeful that this research will help us further understand the structural and genetic ties to Alzheimer's disease and perhaps offer clues that may help us develop new drugs or therapies."

This study could help lead the way to developing better tools for earlier detection rather than relying heavily on evaluations of thought process through mental tests. All studies seem completely worthwhile when up against a degenerative and terminal disease that has no cure and affects millions worldwide every year.

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