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Does It Matter?

Today is National Certified Nurses Day and we want to pay homage to those who are committed to advancing their knowledge and skills in nursing toward becoming experts in their field.

Certification is a result of hard work, dedication and commitment to the highest standards of nursing and these nurses are a credit to the entire field. It means they have continued their professional development, can assure the public and employers they are current in their knowledge and can deliver top-notch care. http://www.medscape.com/viewarticle/564133

But this kind of pursuit in nursing goes much further than credentials. It is also a dedication of caring that sets them apart. Although many already had an innate ability for being an advocate to those around them, it is unique training and learning opportunities along the way that uplift and help a nurse never forget why they wanted to go into nursing in the first place.

It’s been said that a nurse is “one of the few blessings of being ill” (Sara Moss-Wolfe). We know without a doubt that nurses are truly a blessing! What a privilege it is to work with people who are devoted not only to their highest proficiency in nursing, but who truly are “advocates in the care of individuals, families, communities, and populations.” (American Nurses Association)

Happy Certified Nurses Day!

(Image source: https://geronurseprep.com/blog/happy-certified-nurses-day/)

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I’ve Retired, Now What?

It’s a common question for many and the reason why some are actually scared of the thought of retirement. Let’s face it, after a lifetime of hard work, the Monday through Friday rat race, you have embarked on a whole new lifestyle you may find you weren’t totally prepared for. Many may fear finding things to keep them busy throughout the day or making new friends. For others the mere reality of getting older and not wanting to be a burden is a frightening prospect. This is especially true for those whose spouses have died, are sick, or have little or no family near to rely on.

When that point has been reached and you’re not sure how to embark on this retired road, we are here to help you on your journey. Care Patrol is made up of real people who are professionals in helping people make better senior living choices. We personally “match” our clients with a lifestyle to fit individual needs, while protecting their personal information. Because Care Patrol’s services are available nationwide, we are able to aid our clients in finding a lifestyle where they will feel comfortable and cared for from retired living, assisted living and more.

Senior care comes in so many shapes and sizes, you deserve more than just a random list! With our personal, quality service, there is just no reason anyone has to travel this road alone. Call Care Patrol today at (866) 560-5656 to stop searching and start finding!

(Image source: http://glutenfreeville.com)

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Alzheimer's Association Educational Video

Do you know the 10 warning signs of Alzheimer's Disease? Are you aware of the plight of caregivers -- the friends and loved ones who care for Alzheimer's patients? These topics and more are covered in this presentation from the Alzheimer's Association.

www.carepatrol.com

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Therapy Dog Bringing Comfort To Nursing Home

A blog was posted here a while back about the use of therapy canines with the elderly living in assisted and memory care facilities.  Thought it would be nice to share this story that was on NBC's Today Show on June 26, 2013. Here is veteran NBC journalist Jane Pauley and her one on one with Sue Halperin about her canine Pransky and the preparation that was included with Sue's dog turning into a therapy pooch.

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Alzheimer’s and Mentoring Children

The exact cause of Alzheimer’s is still not totally understood but medical researchers know it involves the brain’s memory, language and thought processes. Currently, there is no cure or medication that proves to be beneficial with Alzheimer’s disease. However, medical experts do believe that taking part in social functions on a regular basis will help keep the mind active. Early stage Alzheimer’s patients should be encouraged to seek out and participate in intellectually stimulating activities including reading, doing crossword puzzles, number/word games or taking an interest course.

Another highly beneficial activity those afflicted with the early stages of Alzheimer’s is being a mentor to children. Doing so can effectively boosts a patient’s morale and encourages mental activity. A school age child’s extra-curricular activities can involve spending quality time with an early stage Alzheimer’s patient. The patient could be a family member, friend or someone recommended by a local Alzheimer’s society.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 – days, evenings or weekends! Find us online at http://www.carepatrol.com/.

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Medications Are Common Cause Of Senior Falls

One of the unfortunate consequences of aging is sluggish blood flow to your brain. This means that even though you’re eating the right foods, your brain may not be receiving all the nutrients it desperately needs to function at its best. There’s a natural solution to this problem in a specific nutrient called vinpocetine. This natural compound comes from the periwinkle plant and is used all over the world to treat vascular dementia and other cognitive disorders.

Vinpocetine works by dilating (opening up) the blood vessels to enhance blood flow to specific regions of the brain and improve the utilization of glucose and oxygen. It increases energy metabolism in the brain and even helps to reduce blood clotting, making it an effective deterrent to stroke. In people with Alzheimer’s disease, age-related memory decline and stroke, vinpocetine has been shown to enhance overall brain function and cognitive ability. It appears to work by increasing healthy blood flow to the entire damaged region of the brain.

In Europe where vinpocetine is sold under the brand name Cavinton, 75 to 80% of people with various cerebrovascular disorders have shown improvement on measures of cognitive function.(1) In a study of elderly people with chronic cerebral dysfunction, 42 patients were givien 10 mg of vinpocetine three times a day for 30 days, then 5 mg three times a day for 60 days. Placebo tablets were given to another 42 patients for the 90-day trial period. Patients on vinpocetine scored consistently better in all evaluations, including measurements on the Clinical Global Impression (CGI) scale, the Sandoz Clinical Assessment Geriatric (SCAG) scale, and the Mini-Mental Status Questionnaire (MMSQ).

No serious side effects were noted.(2) More recent studies indicate that vinpocetine also offers direct protection against neurological aging. It has been shown to maintain electrical conduction between brain cells and to provide protection from damage caused by excessive intracellular release of calcium.(2) As a potent natural antioxidant, vinpocetine reduces oxidative stress and the free radicals that can damage delicate brain cells.

In order to derive the greatest benefits from vinpocetine’s ability to improve cerebral blood flow, it is important to ensure you are consuming a brain-healthy diet. Be sure to include generous daily servings of essential fatty acids, antioxidant-rich fruits and vegetables, and B-vitamin-boosting whole grains along with a daily dose of vinpocetine. While you’re taking vinpocetine you’ll be pleased to know that its benefits go far beyond brain health. One study showed that it protects the retina from the hepatitis B virus. In animal studies, vinpocetine was shown to protect against gastric lesions caused by excessive alcohol consumption.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 – days, evenings or weekends! Find us online at http://www.carepatrol.com/.

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Medications Are Common Cause Of Senior Falls

Did you know that medications are a common cause of falling among older adults? Be especially wary of new prescriptions or changes in existing prescriptions, such as a new dosage. Sometimes specialists alter a medication without the rest of a medical team knowing, and even a slight change in dosage or a new combination of medications can create symptoms that contribute to falls.Symptoms include dizziness, drowsiness, unsteadiness, and loss of consciousness.

Meds to watch out for in particular: over-the-counter antihistamines and sleep aids (including the PM version of common painkillers), antipsychotics and antianxiety drugs, and drugs for overactive bladder. Blood-pressure medications pose a special risk when dosages are being adjusted; falls are more likely when the dose is too high.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

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6 Power-Napping Secrets For Caregivers

Sleep deprivation is a special risk for caregivers. Napping can help you recharge your brain and body. These napping tricks can help:

Time it right. After lunch is a good nap time for most people because it meshes with your natural circadian rhythms. Some of your deepest sleep comes between 1 a.m. and 3 a.m., and you’re naturally sleepy again 12 hours later.

Take a driveway nap. Sounds crazy, but when you have time off for errands because someone else is with your loved one, don’t rush back into the house afterward. If you need some sleep, pull into the driveway and catch some shut-eye for ten minutes right there.

Try “co-napping.” If your loved one naps during the day, resist the urge to get a million other things done — try to catnap yourself at the same time. If the person in your care isn’t a napper, try setting up a reclining chair in his or her room so that you can be together while, say, watching TV — but you can also nod off for a spell.

Use a timer. Experienced power-nappers can rouse themselves after just 10 or 15 minutes, but you may need the help of an alarm. The ideal nap is less than 20 minutes long — sleep longer and you may awaken groggy and disoriented, and find that your nighttime sleep is affected. When the alarm goes off, resist the urge to drowse; get up right away.

Take a “caffeine nap.” Drink a cup of caffeinated coffee, then take a 15-minute nap immediately after. It sounds backward, but research shows that this particular combination makes you feel more alert and recharged than if you just drank the coffee, or just napped for 15 to 30 minutes. Called a “caffeine nap,” it gives you the refreshing effects of sleep plus a jolt of caffeine, which kicks in just as you’re waking up.

Use sleep cues. Some sleep experts advise against napping in your bed, because it signals you to fall into a longer, deeper sleep than you need for napping. But it’s still a good idea to use other sleep cues: a darkened room, quiet (turn off the TV if you can), and a blanket to lull your body to a cozy sleep temperature.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

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5 Signs of Alzheimer’s That Sometimes Show up Before Memory Loss

Forgetfulness isn't always the first sign of dementia

Memory loss is the symptom everybody worried about Alzheimer’s disease or other forms of dementia seems to focus on. After all, it’s distressing — and increasingly obvious. Yet there are other common symptoms of Alzheimer’s or dementia that can turn up even earlier, researchers say.

Sometimes, according to memory experts, even doctors miss early dementia signs because they’re focused on memory loss to the exclusion of other symptoms.

In fact, in 2011 Spanish researchers found that more than a third of adults who go on to develop early-onset Alzheimer’s (the kind that appears before age 65) have the following symptoms early in the disease, even before memory loss is apparent. These symptoms can also be the first to appear among adults who develop Alzheimer’s after age 65.

Of course, if you notice any of these symptoms, it’s important to have them checked out by a doctor, psychologist, or other expert in cognition and the brain.

Early sign of dementia #1: Personality change

A warm, friendly loved one may seem to morph into a bit of a grouch — at first occasionally, and then increasingly. A gregarious person still jokes and talks a lot but begins to say inappropriate things or make odd accusations. A mild-mannered loved one begins cursing. All of these are examples of the kinds of personality changes that can predate memory loss in someone with dementia. Often, it’s only later that friends and family look back and realize that behaviors they found off-putting or upsetting weren’t intentional but related to the Alzheimer’s.

Early sign of dementia #2: Problems with executive functioning

Trouble carrying out basic, familiar tasks can creep up slowly but surely. The person may, for example, have difficulty doing something that involves multiple steps, like following written directions or instructions. A longtime cook may avoid complicated recipes. A hobbyist may simplify the form of his or her craft.

Other hallmark trouble areas: making plans and not following through, whether for a vacation or an activity. Not tracking bills. Not being able to solve simple problems, such as mending a broken piece of machinery he or she could once fix easily.

Early sign of dementia #3: Vision problems

Problems with depth perception or visual-spatial coordination can precede memory problems. The person may have trouble driving or even walking well without tripping on stairs. It can be hard to judge distances or see contrasts between like colors, which can lead to accidents. In a more severe example of a perception problem, the person may not recognize himself or herself in a mirror or when passing his or her reflection in a building or window on the street.

Early sign of dementia #4: Language problems

Word retrieval and getting out the right words can become apparent before friends and family notice the more common communication problem of repeating stories or questions. For example the person having trouble may stop in the middle of a sentence, unable to think of the next word. (This can happen to anyone, but when it’s a sign of dementia, it happens with alarming frequency, and sometimes the person isn’t even aware of doing it.) Or the wrong word may come out — “mouth cleaner” for “toothbrush” or “picture stick” for “TV remote control.”

Early sign of dementia #5: Social withdrawal

Early in Alzheimer’s disease and other dementia's, the person is often well aware that something is amiss, even if he or she isn’t exactly sure of the source of the problem. It can be frightening to feel that you’re not quite in control of your faculties all of the time. This can cause the person to use more and more energy to stay in self-command. That leaves less energy to interact with others. Sometimes the person isn’t even aware that he or she seems to be losing interest in friends and family, because he or she is concentrating so hard on just getting through the day.

Social withdrawal can also be caused by a desire to avoid embarrassment or by depression – which often develops alongside dementia.

Social withdrawal can also be caused by a desire to avoid embarrassment or by depression – which often develops alongside dementia. Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

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Alzheimer's Drug Discovery: Looking Under The Right ROCK

A discovery by Emory Alzheimer’s Disease Research Center and Scripps Research Institute scientists could lead to drugs that slow Alzheimer’s disease progression.

A straightforward drug strategy against Alzheimer’s is to turn down the brain’s production of beta-amyloid, the key component of the disease’s characteristic plaques. A toxic fragment of a protein found in healthy brains, beta-amyloid accumulates in the brains of people affected by the disease.

The enzyme that determines how much beta-amyloid brain cells generate is called BACE (beta-secretase or beta-site APP cleaving enzyme). Yet finding drugs that inhibit that elusive enzyme has been far from straightforward.

Now researchers have identified a way to shut down production of beta-amyloid by diverting BACE to a different part of the cell and inhibiting its activity. The results were published this week in Journal of Neuroscience.

"This is an indirect but highly effective way of blocking BACE, which controls the chokepoint step in beta-amyloid production," says lead author Jeremy Herskowitz, PhD, instructor in neurology at Emory’s Alzheimer’s Disease Research Center.

"Jeremy has found a promising approach toward reducing beta-amyloid production and potentially modifying Alzheimer’s disease progression, something for which there is immense need," says senior author James Lah, MD, PhD, associate professor of neurology at Emory University School of Medicine and director of the Cognitive Neurology program. "Drugs that reduce beta-amyloid production would probably be mostly preventive. However, since amyloid-beta is toxic, such drugs could have some immediate effect on cognitive impairment."

In the paper, Herskowitz and his colleagues demonstrate that a specific inhibitor of the enzyme ROCK2 can cut beta-amyloid production in brain cells by more than 75 percent. Co-author Yangbo Feng, PhD, associate director of medicinal chemistry at Scripps Research Institute in Florida, previously discovered the ROCK2 inhibitor, called SR3677.

Alzheimer’s researchers were already interested in ROCK2 and a related enzyme, ROCK1, because of a connection with NSAIDs (non-steroid anti-inflammatory drugs) such as ibuprofen. Some NSAIDS can inhibit production of a particularly toxic form of beta-amyloid, and scientists believed NSAIDs were exerting their effects through the ROCKs.

Herskowitz first showed that in cultured cells, “knocking down” the ROCK2 gene reduced beta-amyloid production, but knocking down ROCK1 had the opposite effect.

"This says that anytime you’re hitting both ROCKs at once, the effects cancel each other out," he says.

The known drugs that affect the ROCKs seemed to affect both and thus have diminished effects. In contrast, SR3677 inhibits ROCK2 much more effectively than ROCK1, and it offered a way around the obstacle. Herskowitz found that by inhibiting ROCK2, SR3677 diverts BACE to a different part of the cell, where it is less likely to act on beta-amyloid’s parent protein.

He and ADRC colleagues found that ROCK2 levels are higher than usual in tissue samples from brains of patients with Alzheimer’s, including those with mild cognitive impairment, thought to be a precursor stage of the disease.

"There is plenty of ROCK2 in the brain, and its levels are elevated in Alzheimer’s patients, indicating that it’s an excellent drug target," Herskowitz says. "We are eager to pursue more extensive studies of this strategy in animal models of Alzheimer’s."

SR3677 can substantially inhibit beta-amyloid production in an animal model of Alzheimer’s, but so far, this effect has been observed when the drug is injected directly into the brain. More studies are required to learn if SR3677 or related drugs can pass the blood-brain barrier and thus be given by injection or orally, and what side effects could appear. ROCK inhibitors are also being investigated for treating other conditions such as glaucoma, hypertension and multiple sclerosis. 

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Source: news.emory.edu)

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Alzheimer's Risk Gene May Affect Brain Early As Childhood

People who carry a high-risk gene for Alzheimer’s disease show changes in their brains beginning in childhood, decades before the illness appears, new research from the Centre for Addiction and Mental Health (CAMH) suggests.

The gene, called SORL1, is one of a number of genes linked to an increased risk of late-onset Alzheimer’s disease, the most common form of the illness. SORL1 carries the gene code for the sortilin-like receptor, which is involved in recycling some molecules in the brain before they develop into beta-amyloid a toxic Alzheimer protein. SORL1 is also involved in lipid metabolism, putting it at the heart of the vascular risk pathway for Alzheimer’s disease as well.

“We need to understand where, when and how these Alzheimer’s risk genes affect the brain, by studying the biological pathways through which they work,” says Dr. Aristotle Voineskos, head of the Kimel Family Translational Imaging-Genetics Laboratory at CAMH, who led the study. “Through this knowledge, we can begin to design interventions at the right time, for the right people.” The study was recently published online in Molecular Psychiatry with Dr. Voineskos’s graduate student, Daniel Felsky as first author, and was a collaborative effort with the Zucker Hillside Hospital/Feinstein Institute in New York and the Rush Alzheimer’s Disease Center in Chicago.

To understand SORL1’s effects across the lifespan, the researchers studied individuals both with and without Alzheimer’s disease. Their approach was to identify genetic differences in SORL1, and see if there was a link to Alzheimer’s-related changes in the brain, using imaging as well as post-mortem tissue analysis.

In each approach, a link was confirmed.

In the first group of healthy individuals, aged eight to 86, researchers used a brain imaging technique called diffusion tensor imaging (DTI). Even among the youngest participants in the study, those with a specific copy of SORL1 showed a reduction in white matter connections in the brain important for memory performance and executive function. 

The second sample included post-mortem brain tissue from 189 individuals less than a year old to 92 years, without Alzheimer’s disease. Among those with that same copy of the SORL1 gene, the brain tissue showed a disruption in the process by which the gene translated its code to become the sortilin-like receptor.

Finally, the third set of post-mortem brains came from 710 individuals, aged 66 to 108, of whom the majority had mild cognitive impairment or Alzheimer’s. In this case, the SORL1 risk gene was linked with the presence of amyloid-beta, a protein found in Alzheimer’s disease. 

Dr. Voineskos notes that risk for Alzheimer’s disease results from a combination of factors – unhealthy diet, lack of exercise, smoking, high blood pressure combined with a person’s genetic profile – which all contribute to the development of the illness. “The gene has a relatively small effect, but the changes are reliable, and may represent one ‘hit’, among a pathway of hits required to develop Alzheimer’s disease later in life”.

While it’s too early to provide interventions that may target these changes, “individuals can take measures in their own lifestyle to reduce the risk of late-onset Alzheimer’s disease.” Determining whether there is an interaction with this risk gene and lifestyle factors will be one important next step.

In order to develop genetically-based interventions to prevent Alzheimer’s disease, the biological pathways of other risk genes also need to be systematically analyzed, the researchers note.

This research does, however, build on a previous CAMH imaging-genetics study on another gene related to Alzheimer’s disease. That study showed that a genetic variation of brain-derived neurotrophic factor (BDNF) affected brain structures in Alzheimer’s.

“The interesting connection is that BDNF may have important therapeutic value. But there is data to suggest that the effects of BDNF won’t work unless SORL1 is present, so there is the possibility that if you boost the activity of one gene, the other will increase,” says Dr. Voineskos, adding that BDNF therapeutics are in development. A next stage in the research, he says, is to look at the interaction of BDNF and SORL1.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Source: camh.ca)

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Brain Imaging Differences In Infants At Genetic Risk For Alzheimer's

Researchers from Brown University and Banner Alzheimer’s Institute have found that infants who carry a gene associated with increased risk for Alzheimer’s disease tend to have differences in brain development compared to children without the gene. The study, published in JAMA Neurology, demonstrates some of the earliest developmental differences associated with a gene variant called APOE ε4, a common genotype and a known risk factor for late-onset Alzheimer’s.

The researchers imaged the brains of 162 healthy infants between the ages of two months and 25 months. All of the infants had DNA tests to see which variant of the APOE gene they carried. Sixty of them had the ε4 variant that has been linked to an increased risk of Alzheimer’s. Using a specialized MRI technique, the researchers compared the brains of ε4 carriers with non-carriers. They found that children who carry the APOE ε4 gene tended to have increased brain growth in areas in the frontal lobe, and decreased growth in areas in several areas in the middle and rear of the brain. The decreased growth was found in areas that tend to be affected in elderly patients who have Alzheimer’s disease.

Researchers emphasized that the findings do not mean that any of the children in the study are destined to develop Alzheimer’s or that the brain changes detected are the first clinical signs of the disease. What the findings do suggest, however, is that brains of APOE ε4 carriers tend to develop differently from those of non-ε4 carriers beginning very early in life. It is possible that these early changes provide a “foothold” for the later pathologies that lead to Alzheimer’s symptoms, the researchers say. Information from this study may be an important step toward understanding how this gene confers risk for Alzheimer’s, something that is not currently well understood.

“This work is about understanding how this gene influences brain development,” said Sean Deoni, who oversees Brown University’s Advanced Baby Imaging Lab and was one of the study’s senior authors. “These results do not establish a direct link to the changes seen in Alzheimer’s patients, but with more research they may tell us something about how the gene contributes to Alzheimer’s risk later in life.”

The APOE ε4 variant linked to Alzheimer’s is present in about 25 percent of the U.S. population. Not everyone who carries the gene gets Alzheimer’s, but 60 percent of people who develop the disease have at least one copy of the ε4 gene.

The gene is thought to have several different roles in the blood and brain, some of which remain to be clarified. For instance, it has been shown to participate in regulation of cholesterol, a molecule that is involved in the development of gray matter and white matter brain cells. It has also been shown to participate in the regulation of amyloid, a brain protein that accumulates in Alzheimer’s and is now being targeted by investigational treatments. Studies are needed to clarify the ways in which APOE, human development, aging and other risk factors may conspire to produce the brain changes involved in Alzheimer’s disease.

The researchers used an MRI technique developed at Brown’s Advanced Baby Imaging Lab. The technique quiets the MRI machine to a whisper, enabling the brains of healthy babies to be imaged while they sleep without medication. The technique also enables imaging of both gray matter — the part of the brain that contains neurons and nerve fibers — and white matter, which contains the fatty material that insulates the nerve fibers. Both gray and white matter are thought to have a role in Alzheimer’s. White matter growth begins shortly after birth and is an important measure of brain development.

“We’re in a good spot to be able to investigate how this gene influences development in healthy infants,” said Deoni, assistant professor of engineering at Brown. “These infants are not medicated and not showing any cognitive decline — quite the opposite, actually; they’re developing normally.”

There is no reason to believe that the children won’t continue to develop normally, Deoni said. There is no consistent evidence to suggest that ε4 carriers suffer any cognitive problems or developmental delay. And the areas of increased growth raise the possibility that the gene might actually confer some advantages to infants early on. Utimately the researchers hope the findings could lead to new strategies for preventing a disease that currently affects more than 5.2 million people in the U.S. alone.

“It may sound scary that we could detect these brain differences in infants,” said Dr. Eric Reiman, executive director of the Banner Alzheimer’s Institute in Arizona and another senior author on the paper. “But it is our sincere hope that an understanding of the earliest brain changes involved in the predisposition to Alzheimer’s will help researchers find treatments to prevent the clinical onset of Alzheimer’s disease — and do so long before these children become senior citizens.”

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Source:  NueroScience)

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Insight Into How Our Memories Form Could Help Treat Dementia

Do fruit flies hold the key to treating dementia? Researchers at the University of Houston (UH) have taken a significant step forward in unraveling the mechanisms of Pavlovian conditioning. Their work will help them understand how memories form and, ultimately, provide better treatments to improve memory in all ages.

Gregg Roman, an associate professor of biology and biochemistry at UH, and Shixing Zhang, his postdoctoral associate, describe their findings in a paper titled “Presynaptic Inhibition of Gamma Lobe Neurons Is Required for Olfactory Learning in Drosophila,” appearing Nov. 27 in Current Biology, a scientific bimonthly journal published by Cell Press.

“Memory is essential to our daily function and is also central to our sense of self,” Roman said. “To a large degree, we are the sum of our experiences. When memories can no longer be retrieved or we have difficulty in forming new memories, the effects are frequently tragic. In the future, our work will enable us to have a better understanding of how human memories form.”

Roman and Zhang set about to unravel some of these mysteries by studying the brains of fruit flies (Drosophila). Within the fly brain, Roman says, there are nerve cells that play a role in olfactory learning and memory. Olfactory learning, he says, is an example of classical conditioning first described by Pavlov in his experiment with dogs. In their study, the flies were trained to associate a weak electric shock with an odor. After training, the flies avoided that odor.

“We found that these particular nerve cells – the gamma lobe neurons of the mushroom bodies in the insect brain – are activated by odors. Training the flies to associate an odor with an electric shock changed how these cells responded to odors by developing a modification in gamma lobe neuron activity, known as a memory trace,” he said. “Interestingly, we found that training caused the gamma lobe neurons to be more weakly activated by odors that were not paired with an electric shock, while the odors paired with electric shock maintained a strong activation of these neurons. Thus, the gamma lobe neurons responded more strongly to the trained odor than to the untrained odor.”

The team also showed that a specific protein – the heterotrimeric G(o) protein – is naturally involved in inhibiting gamma lobe neurons. Roman says removing the activity of this protein only within the gamma lobe neurons resulted in a loss of the memory trace and, thus, poor learning. Therefore, inhibiting the release of neurotransmitters from these neurons through the actions of the G(o) protein is key to forming the memory trace and associative memories.

The significance of using fruit flies is that while their brain structure is much simpler with far fewer neurons, the mushroom body is analogous to the perirhinal cortex in humans, which serves the same function of sensory integration and learning. This simplicity allows scientists to gain insights into how memories are acquired, stored and retrieved.

“Drosophila represents the Goldilocks principle of neural research, with sufficient behavioral complexity, while maintaining a huge advantage in neural simplicity,” Roman said. “The complex behaviors allow us to examine many behavioral processes like learning, attention, aggression and addiction-like behaviors, while the simplicity allows us to dissect the crucial neural activities down to single cells. Additionally, Drosophila has the most powerful genetic toolkit available for behavioral experimentation. In using these tools, we are genetically identifying the molecules necessary to perform these behaviors and dissecting the logic of the neural circuits that allow for changes in behavior to occur.”

The pair says all their experience to date suggests the molecules and logic will translate to most animals, including humans, leading to a more complete understanding of how memories form in humans, both at the level of molecules and through the activity of neural circuits.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

  (Source: NueroScience)

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Broken Cellular "Clock" Linked To Brain Damage

A new discovery may help explain the surprisingly strong connections between sleep problems and neurodegenerative conditions such as Alzheimer’s disease. Sleep loss increases the risk of Alzheimer’s disease, and disrupted sleeping patterns are among the first signs of this devastating disorder.

Scientists at Washington University School of Medicine in St. Louis and the University of Pennsylvania have shown that brain cell damage similar to that seen in Alzheimer’s disease and other disorders results when a gene that controls the sleep-wake cycle and other bodily rhythms is disabled.

The researchers found evidence that disabling a circadian clock gene that controls the daily rhythms of many bodily processes blocks a part of the brain’s housekeeping cycle that neutralizes dangerous chemicals known as free radicals.

“Normally in the hours leading up to midday, the brain increases its production of certain antioxidant enzymes, which help clean up free radicals,” said first author Erik Musiek, MD, PhD, assistant professor of neurology at the School of Medicine. “When clock genes are disabled, though, this surge no longer occurs, and the free radicals may linger in the brain and cause more damage.”

Musiek conducted the research in the labs of Garret FitzGerald, MD, chairman of pharmacology at the University of Pennsylvania, and of David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology at Washington University School of Medicine, who are co-senior authors.

The study appears Nov. 25 in The Journal of Clinical Investigation.

Musiek studied mice lacking a master clock gene called Bmal1. Without this gene, activities that normally occur at particular times of day are disrupted.

“For example, mice normally are active at night and asleep during the day, but when Bmal1 is missing, they sleep equally in the day and in the night, with no circadian rhythm,” Musiek said. “They get the same amount of sleep, but it’s spread over the whole day. Rhythms in the way genes are expressed are lost.”

FitzGerald uses mice lacking Bmal1 to study whether clock cells have links to diabetes and heart disease. He has shown that clock genes influence blood pressure, blood sugar and lipid levels.

Several years ago, Musiek, who at the time was a neurology resident at the University of Pennsylvania, and FitzGerald decided to investigate how knocking out Bmal1 affects the brain. Holtzman, who has published pioneering work on sleep and Alzheimer’s disease, encouraged Musiek to continue and expand these studies when he came to Washington University as a postdoctoral fellow.

In the new study, Musiek found that as the mice aged, many of their brain cells became damaged and did not function normally. The patterns of damage were similar to those seen in Alzheimer’s disease and other neurodegenerative disorders.

“Brain cell injury in these mice far exceeded that normally seen in aging mice,” Musiek said. “Many of the injuries appear to be caused by free radicals, which are byproducts of metabolism. If free radicals come into contact with brain cells or other tissue, they can cause damaging chemical reactions.”

This led Musiek to examine the production of key antioxidant enzymes, which usually neutralize and help clear free radicals from the brain, thereby limiting damage. He found levels of several antioxidant proteins peak in the middle of the day in healthy mice. However, this surge is absent in mice lacking Bmal1. Without the surge, free radicals may remain in the brain longer, contributing to the damage Musiek observed.

“We’re trying to identify more specifics about how problems in clock genes contribute to neurodegeneration, both with and without influencing sleep,” Musiek said. “That’s a challenging distinction to make, but it needs to be made because clock genes appear to control many other functions in the brain in addition to sleeping and waking.”

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Source: news.wustl.edu)

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How To Get A Person Suffering From Alzheimer's Disease To Take Their Medication?

Anyone who is a caregiver for someone afflicted with Alzheimer's or dementia can explain to you the difficulties they face sometimes when giving the patient their medication.

Bob DeMarco of The Alzheimer's Reading Room offers us some insight into making medication time less stressful.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Image Source: Alzheimer's Reading Room)

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Active Seniors Less Likely For Fractures

A recent study published online in the prestigious journal Osteoporosis International shows that seniors who make healthy changes in their everyday activity to include exercise, taking supplements and even proper footwear, are less likely for the risk of bone fractures.

Dr. Joanna Sale, Clinical Epidemiologist at St. Michaels Hospital in Toronto, Canada, conducted the study with seniors over 65 who were participants in the hospitals Osteoporosis Exemplary Care Program.

Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Image Source: Shutterstock)

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GPS Tracking For Alzheimer's Patients

Most of us have seen news reports regarding a senior that is diagnosed with Alzheimer’s that has wandered or driven away from an assisted living community or their own home. 

This can be a frightening and stressful experience for family, friends and caregivers, especially in regions where the outside temperatures can reach over 100 degrees this time of year.  Also there are concerns that the patient could possibly become the victim of an assault or robbery is of great concern.

The Alzheimer’s Association, in partnership with Omnilink, has a web-based GPS management service called Comfort Zone® which families can use to remotely monitor a loved one by receiving alerts 24 hours a day when the patient has traveled past a pre-set zone.

At CarePatrol we know that the safety and security of your loved one is of the utmost importance. Search nursing home facilities, assisted care, independent living communities, or other care options to find the right fit for your loved one! To speak with a CarePatrol qualified Senior Advisor, call (866) 560-5656 - days, evenings or weekends! Find us online at http://www.carepatrol.com/.

(Image Source: MSN)