Memory and Focus

Many people have problems with memory and focus as they age.  Whether the problems are the beginning stages of dementia or just a lack of focus, the following exercise can help to ensure that aging has less power to rob you of precious memories.  In addition, this exercise provides a possible solution for insomnia.

1.  Focus on the events of the day in order from arising in the morning until you go to sleep. The good news is that you will fall asleep long before you reach the end of the day.

2.  During the process, visualize each step of the day.  The process should include all activities, conversations, thoughts and individuals met during the day.  It might be seen as a video recording of the day played back only in your brain.  Focus on details.

3.  Initially, the mind video will be playing in fast forward.  It will be difficult to pick out the small details such as thinking over your today list or looking in the mirror while brushing one’s teeth.  In addition, scenes may jump out of sequence from morning to afternoon and then back to getting out of bed.  However, your goal is to play the video in sequence.

4.  As you continue the exercise several days in a row, you should begin to see some differences.  That which was once a just big chunk of time will begin to develop into fully visualized scenes, which include people, conversations, room decor, signs and thoughts.  Details will become clearer.

5.  It should become a daily challenge to remember more of the day.  You will become more aware of the things you normally would have done without much thought.  Since you know you must recall, your focus changes.  You are using brain cells not previously harnessed.  While the nighttime exercises may be a cure for insomnia, the daytime exercises help you to focus, improve your memory, and lower the chances of developing dementia.

By improving one’s daytime focus and recalling events of the day, it is possible for people to avoid memory loss and dementia.  Additionally, these activities can help with insomnia.

The ideas in this article are adapted from a blog on how to become a better chess player, but certainly seem appropriate for anyone concerned with dementia and having problems with memory and focus.


One of the distinguishing characteristics of Alzheimer’s disease (AD) is the destruction of brain cells that lead to diminished brain function. Scientists from the University of California at Santa Barbara have discovered what actually happens to these cells in patients with Alzheimer’s and other types of dementia. The findings of the study have been published in The Journal of Biological Chemistry online version.

According to senior author Stuart Feinstein, Ph.D, co-director of UCSB’s Neuroscience Research Institute, brain cells (also known as neurons) stop working properly. Neurons are essential for an individual to perform cognitive skills. The loss of neuronal capacity signals the onset of dementia.

Feinstein, a Molecular, Cellular and Developmental Biology professor, had spent 30 years studying the ‘tau’ protein utilizing cultured cells and test tube bio-chemistry models. Tau is present in long axons which are responsible for connecting neurons and their specific targets. Tau proteins also stabilize microtubules, a component of the cells’ cytoskeleton which is critical to the function and structure of neuronal cells.

For years, it was known that amyloid beta, a type of peptide, can cause the death of neuronal cells and lead to Alzheimer’s disease. The only problem is that it has never been understood how the mechanism that triggers it works. Recent research has shown that amyloid beta requires tau in order to destroy neurons. What is not clear is how it does the action. Most researchers believe that it triggers the excessive chemical modification of tau proteins. For Feinstein, the important goal was to discover the exact details involved in the process of abnormal phosphorylation. By determining what exactly happens, drug companies would have sufficient clues to make the right decisions and pharmaceutical solutions for the problem.

But there is a glitch. The initial hypothesis regarding the effect of amyloid beta on tau phosphorylation was incorrect. What the team discovered was that taking neuronal cells and adding amyloid beta did not result in massively phosphorylated tau proteins. Instead, it resulted in the fragmentation of the proteins within one to two hours and the death of the cells within 24 hours.

According to Feinstein, tau performs multiple jobs, the most widely understood of which is the regulation of cellular cytoskeleton. Cell skeletons, unlike human skeletons, do not undergo abrupt change in its shape. Cell skeletons constantly move, grow and shorten to allow the cell to perform its many functions. The length of cytoskeleton is essential to neurons due to its length.

After the findings, Feinstein’s argument is that the death of neurons that occur in Alzheimer’s is due to a malfunctioning cytoskeleton and that destroying tau proteins can lead to cell death. Feinstein hypothesized the same action that destroys the cytoskeleton in cells treated with cancer drugs could be the same action that was triggered in the neuronal cells.

According to an article published in Translational Neuroscience, a study done at the Mount Sinai School of Medicine found that patients with Alzheimer’s disease (AD) have lower glucose utilization in the brain than those with normal cognitive function. The decreased levels could possibly be detected 20 years prior to the first symptoms of AD. With this knowledge comes the possibility of developing new therapies of preventing the start of Alzheimer’s.

In the article reported at (, the study used mice modified to develop Alzheimer’s disease. The research team found that when β-amyloid, an abnormal protein linked to Alzheimer’s disease, starts to become detectable in the brain in its soluble toxic form, the mitochondria, or “power plants” of the cell where glucose is converted into energy, became impaired. Within the equivalent of about 20 human years, mice with decreased energy metabolism developed signs of Alzheimer’s disease such as cognitive defects and impairment of the synaptic terminal, the area of brain cells important in memory formation.

“This evidence in mice validates that the diagnosis of probable Alzheimer’s disease may be the end result of impairment in brain cell energy production,” said the study’s lead author, Giulio M. Pasinetti, MD, PhD, The Saunder Family Professor in Neurology, and Professor of Psychiatry, Geriatrics, and Adult Development at Mount Sinai School of Medicine. “Identifying that mitochondrial impairment is evident years earlier than cognitive defects is a major breakthrough.”

“This new evidence could revolutionize the way we design interventions,” said Merina T. Varghese, MD, co-author of the study and Postdoctoral Fellow in Neurology at Mount Sinai School of Medicine. “This study sets the stage for the development of potential novel preventions or therapies to apply in humans, even when they have normal cognitive function, to prevent the eventual onset of Alzheimer’s disease.”

Enhanced by Zemanta

Researchers at the University of South Florida’s Department of Psychiatry and the Center of Excellence for Aging and Brain Repair have discovered that the CD45 molecule, a receptor on the surface of the brain’s microglia cells (cells that support the brain’s neurons and also participate in brain immune responses) is a new focus for the prevention of detrimental immune responses which are determined as elements in the development of Alzheimer’s disease (AD). Their findings were reported in the Journal of Neuroscience.

Previous studies by the USF researchers demonstrated that triggering CD45 was advantageous because it blocked a very early step in the development of Alzheimer’s disease. In the current study, the researchers showed in Alzheimer’s mouse models that a loss of CD45 led to dramatically increased microglial inflammation.

Although the brain’s immune response is associated with Alzheimer’s disease pathology, “this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation,” said study senior author Jun Tan, MD, PhD, a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran’s Hospital.

The investigators also found a raised level of harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.

“In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer’s mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons,” Dr. Tan said. “These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor.”

The next step is to apply these findings to develop new Alzheimer’s disease treatments, said Paula Bickford, PhD, a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran’s Hospital. “We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain’s immune cells,” Dr. Bickford said.

Enhanced by Zemanta

Most people did not believe Columbus when he said the world is round. Now in the world of Alzheimer’s disease research, Sam Gandy, M.D., Ph.D., Professor of Neurology and Psychiatry, and Associate Director of the Alzheimer’s Disease Research Center, Mount Sinai School of Medicine, has created quite a stir. He states, “The buildup of amyloid plaques was described over 100 years ago and has received the bulk of the attention in Alzheimer’s pathology. But there has been a longstanding debate over whether plaques are toxic, protective, or inert.”

So instead of the belief that brain cells are being destroyed by the sticky plaques, Gandy and his researchers think that there are free-floating clumps of protein that may be the culprit and that the sticky plaques may actually be protecting the body against these toxic clumps.

According to the Mount Sinai School of Medicine:

Several research groups had previously proposed that rather than plaques, floating clumps of amyloid (called oligomers) are the key components that impede brain cell function in Alzheimer’s patients. To study this, the Mount Sinai team developed a mouse that forms only these oligomers, and never any plaques, throughout their lives.

The researchers found that the mice that never develop plaques were just as impaired by the disease as mice with both plaques and oligomers. Moreover, when a gene that converted oligomers into plaques was added to the mice, the mice were no more impaired than they had been before.

This will take research in a new direction. Drugs that target plaques may not be of any help and could even make the disease worse.  Gandy works with specially engineered mice and William Thies, Chief Medical Officer, Alzheimer’s Association, warns us that the leap from mice to men is a long one and until Gandy’s experiments can be duplicated, drug companies will not be investing billios of dollars into creating new medication.

When Andrew Dillin, Ph.D., of the Salk Institute for Biological Studies started pursuing the oligomer theory several years ago, he said the the idea was so controversial that some scientists would walk out of the room when he made his presentations at conferences. Now, many top researchers are convinced.

More about oligomers and plaques in the next post.

Enhanced by Zemanta

10 Ways to Maintain Your Brain

The Alzheimer’s Association has a booklet called, Maintain Your Brain, and subtitled — there is growing evidence that lifestyle can affect your brain health. You can obtain this 16-page online booklet by clicking here. If you want a quick summary, the 10 ways to maintain your brain discussed are:

  1. Head first
    Good health starts with your brain. It’s one of the most vital body organs, and it needs care and maintenance.
  2. Take brain health to heart
    What’s good for the heart is good for the brain. Do something every day to prevent heart disease, high blood pressure, diabetes and stroke — all of which can increase your risk of Alzheimer’s.
  3. Your numbers count
    Keep your body weight, blood pressure, cholesterol and blood sugar levels within recommended ranges.
  4. Feed your brain
    Eat less fat and more antioxidant-rich foods.
  5. Work your body
    Physical exercise keeps the blood flowing and may encourage new brain cells. Do what you can — like walking 30 minutes a day — to keep both body and mind active.
  6. Jog your mind
    Keeping your brain active and engaged increases its vitality and builds reserves of brain cells and connections. Read, write, play games, learn new things, do crossword puzzles.
  7. Connect with others
    Leisure activities that combine physical, mental and social elements may be most likely to prevent dementia. Be social, converse, volunteer, join a club or take a class.
  8. Heads up! Protect your brain
    Take precautions against head injuries. Use your car seat belts, unclutter your house to avoid falls, and wear a helmet when cycling or in-line skating.
  9. Use your head
    Avoid unhealthy habits. Don’t smoke, drink excessive alcohol or use street drugs.
  10. Think ahead — start today!
    You can do something today to protect your tomorrow.
Enhanced by Zemanta

Center for Molecular and Behavioral Neuroscience

The Center for Neuroscience at Rutgers University – Newark publishes a wonderful newsletter, Memory Loss and the Brain. In the Winter 2010 issue, one of the articles is on Parkinson’s disease. Although Parkinson’s is known as a movement disorder which affects how they walk  — slowly with a stiff gait — as well as possibly producing tremors, it also affects memory, learning, and behavior. Alzheimer’s disease and Parkinson’s disease have similarities such as:

  • Both develop slowly over many years
  • Both tend to develop later in life
  • Both are currently incurable
  • Both affect the brain

As a neurological disorder, Parkinson’s disease affects the part of the brain that controls muscle movement. The neurons that make dopamine, a chemical that helps your body coordinate movements, die. As a neurotransmitter, dopamine is essential for the central nervous system to function. Medications are prescribed that increase the amount and effectiveness of dopamine in the brain. However, medications can cause serious cognitive side effects and even possibly addictions such as gambling and overeating.

Unlike Parkinson’s, the cause of Alzheimer’s disease is not as specific. It may be a composite of causes. Medications are available as mentioned in a previous post, but they only work temporarily to slow down the disease and they don’t address the underlying causes. It is difficult to develop effective treatments when the exact cause is not known.

In both cases, lifestyle choice might make a difference. There is growing evidence that aerobic exercise improves memory and various other brain functions … even modest exercise. Click here to see an amazing video of a Parkinson’s patient riding the bicycle. Besides exercise, a healthy diet — one low in “lousy” cholesterol (LDL) and high in fruits, vegetables, and fatty fish — can help possibly prevent dementia. Mental activities that you enjoy and challenge you is possibly another preventive.

We all hope that cures for Alzheimer’s disease and Parkinson’s disease will be found. In the meantime, we can only do what the evidence tells us might possibly help.

Reblog this post [with Zemanta]

Phosphatidylserine Memory Booster

Last month a friend gave me an issue of  Woman’s World magazine. In it was a tiny article, Ward off Alzheimer’s with the new “Memory” Pill! As the author of this Alzheimer’s disease blog, that certainly caught my attention. It’s called phosphatidyl serine (PS) or more commonly spelled as one word in the scientific community, phosphatidylserine. It says, “it’s a supplement proven to prevent age-related memory loss and help your brain function as if it were 12 years younger!” Now, wouldn’t that catch your attention, too? Could we all use a memory booster?

Since it’s such a short article, let me share the rest of it.

PS helps restore the brain’s supply of acetycholine, a neurotransmitter that’s crucial for memory, reports Thom Lobe, M.D., of Beneveda Medical Group in Beverly Hills, California. In one study, folks who took 100 mg., three times a day, scored 30% higher on memory tests after just 12 weeks! Your Rx: 200 mg. to 300 mg. daily in supplement form (find it in health-food stores). Important: Ask your doctor before taking this or any supplement, especially if you also take an anticoagulant drug.

If phosphatidylserine is such an impressive supplement, shouldn’t all Alzheimer’s patients be on it? According to the Mayo Clinic, “Several studies involving phosphatidylserine indicate a benefit — improved cognitive abilities and behaviors. However, improvements in memory lasted only a few months and were seen in people with the least severe symptoms.” They go on to say that earlier studies were based on brain cells of cows. However, because of concerns about mad cow disease, most manufacturers now produce phosphatidylserine supplements from soy or cabbage derivatives. So it’s not really known if the plant-based supplements are equally effective.

WebMD adds that phosphatidylserine is a chemical that the body can make, but it gets most of what it needs from foods. Side effects include insomnia and upset stomach for doses over 300 mg. They warn that there could be drug interactions. Click here for more information and click on Interactions.

So the old adage, if it’s too good to be true, it probably is, appears to be in effect here. Have you ever taken phosphatidylserine? What is your opinion?