Wednesday, August 30, 2017

Nueroinflammation in Allzheimer's

In the journal Current Aging Science, a research team has reviewed modifiable risk factors for Alzheimer's and Parkinson's diseases. The reviewers focus on the possible role of neuroinflammation (inflammation of the nervous tissue) in neurodegenerative disease mechanisms. Alzheimer's disease and Parkinson's disease are among the most common causes of dementia, and increasingly contribute to morbidity and mortality worldwide. A common hallmark of these two diseases is neuroinflammation, which is initially triggered by the presence of pathological molecular structures associated with these disorders. Chronic neuroinflammation is sustained by persistent activation of the non-neuronal glial cells in the brain, which results in damage or death of neighboring cells, including neurons and glial cells themselves. Persistent neuroinflammation of the brain is hypothesized to contribute to the neurodegeneration observed in Alzheimer's and Parkinson's diseases.

The reviewers note four modifiable risk factors for Alzheimer's and Parkinson's diseases: physical inactivity, vascular disease-related conditions, obesity and type two diabetes mellitus. These modifiable risk factors contribute to neuroinflammation through specific mechanisms that are directly linked to the pathologies of Alzheimer's and Parkinson's diseases. These risk factors are deemed modifiable as their occurrence in the general population can be reduced, or avoided by individuals, through various lifestyle changes, such as improved diet, regular exercise and effective treatment of vascular disease-related conditions such as high blood pressure. This review highlights that the control of the modifiable risk factors is a valid approach for managing the increased incidence of both Alzheimer's and Parkinson's diseases. In addition, the neuroinflammatory mechanisms common to Alzheimer's and Parkinson's diseases are described, which may link the above four common modifiable risk factors with both of these neurodegenerative diseases. A better understanding of the molecular mechanism of neuroinflammation could help identify new therapeutic targets for combating neurodegenerative diseases.

Monday, August 28, 2017

Caregivers of those with Alzheimer's

No matter how much you may care for someone, caring for them when they’re ill is not always easy. Especially when that illness is dementia. If you are trying to care for someone with dementia, this podcast is for you. I talked with Teepa Snow, who is a dementia and Alzheimer’s care specialist. She travels around the world sharing her caregiving wisdom with professionals and families. Now she is sharing it with us.

;

For more information about Teepa and the work she does as well as a wide variety of dementia resources, visit her website teepasnow.com.

Saturday, August 26, 2017

Does chocolate help with vascular dementia

NutritionFacts.org

The sugar in chocolate isn’t good for us; the fat and excess calories in chocolate aren’t good for us; but, “natural cocoa powder can be [considered] a health food.” So, adding cocoa to a smoothie, or oatmeal, or whatever, would be health-promoting. But, ideally, choose unprocessed, un-Dutched cocoa, since the flavanols are what give cocoa its bitterness. So, they try to process cocoa with alkali to destroy them, on purpose. Thus, when it comes to cocoa, “bitter [appears to be] better.”

In my video on chocolate and artery function, I showed how dark chocolate could improve the function of coronary arteries in the heart within two hours of consumption, using fancy angiography. But, there are some blood vessels you can visualize with your eyes—the blood vessels in your eyes. Two hours after eating dark chocolate; significant improvement in the ability of the little veins in your eyes to dilate.

What about the blood vessels in your legs? Peripheral artery disease—atherosclerosis in the arteries feeding your limbs, leading to claudication, a crampy pain in your calf muscles when you try to exercise, due to impaired blood flow. So, maximal walking distance and maximal walking time were studied in 20 peripheral artery disease patients, two hours after eating dark chocolate, with a respectable 85+% cocoa, or after eating wimpy milk chocolate. After the dark chocolate, they could walk about a dozen more yards, and about 17 more seconds, than before the dark chocolate.

But, after the milk chocolate they weren’t even able to walk as far as baseline, and not a single second more. So, there does seem to be something in cocoa that’s helping, but a few seconds here or there aren’t going to cut it.

How about reversing the atherosclerosis—which we didn’t even think possible, until 1977? Wait—what happened in ’77? Dean Ornish didn’t start publishing on heart disease reversal until 1979. Well, actually, the first demonstration of atherosclerosis reversal with a cholesterol-lowering diet and drugs wasn’t on the coronary arteries going to the heart, but rather the femoral arteries, going to the legs.

What about the arteries going to the brain? Well, there’s a noninvasive way to measure arterial function within the brain, using transcranial ultrasound. If you ask someone to hold their breath, the brain says uh-oh, and starts opening up the arteries to increase blood flow to compensate. But, if the arteries in our brain are stiffened and crippled by atherosclerosis, they’re unable to open as much and as fast as they should—and so, are said to have a smaller “breath holding index,” which can be a risk factor for stroke. So, researchers designed an experiment in which they compared the results of a target food to something neutral, like oatmeal. So, did they choose like a spoonful of cocoa powder, or something? No. A randomized crossover trial of oatmeal, versus a “deep-fried Mars bar.”

Wait, why a deep-fried Mars bar? Well, this was published in the Scottish Medical Journal, and, evidently, deep-fried Mars bars are “a snack…strongly [associated] with Scotland.” Wait, is this just an urban legend, or something? No. “627 fish and chip shops in Scotland [were called] to ascertain the delicacy’s availability,” and more than one in five said yeah, we’re selling up to 200 a week. Just follow the signs. Comes out a little something like this. Batter-dipped and deep-dried Snickers bars and pizza were, evidently, less popular. The researchers conclude that it’s “not just an urban [legend]. Encouragingly, [they] did find some evidence of the penetrance of the Mediterranean diet…albeit in the form of deep-fried pizza.”

Could this be contributing to Scotland having among the highest stroke rate in Europe? Well, they put it to the test, and, interestingly, there was a significant drop in men, compared to women. Maybe men are from Mars, women are from Snickers?

Regardless, what about chocolate that’s not deep-fried? There’s been a few population studies that have followed people over time, and found that those who ate chocolate appeared to have lower stroke rates—since confirmed by another study.

But, maybe chocolate consumption just happens to be related to other behaviors that are heart- and brain-healthy? Like hey, people that exercise a lot have to eat more food, period. So, maybe they eat more chocolate? They didn’t see any evidence of that, but you can’t account for everything. To prove cause and effect, you’d have to like randomize people into two groups, and make half eat chocolate, and the other half not, and follow them out for a decade or two—to which one researcher replied, fat chance; you try to get people into a study where they could be randomized to 16 years without chocolate.

Thursday, August 24, 2017

Drug for dementia and osteoporosis

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

Elsevier

The most common drug for Alzheimer's also increases bone mass in mice. Find out what this means for people with dementia in fear of bone fractures, as well as conditions like osteoporosis or periodontitis.

The most common drug used to treat Alzheimer's disease increases bone mass in mice, according to a groundbreaking research article published in the open access journal Heliyon. The authors of the study, from Saitama Medical University in Japan, say this means the drug could also be used to treat bone loss diseases like osteoporosis and periodontitis, following further clinical research.

Alzheimer's disease is the most common form of dementia and the incidence is increasing in our aging population. In the early stages of Alzheimer's disease, bone density decreases, putting patients at a higher risk of bone fractures.

Donepezil (Brand name : Aricept^®)

The new Heliyon study suggests that treating Alzheimer's disease with a drug called donepezil (Brand name : Aricept^®) not only improves cognitive function but also increases bone density, reducing the risk of fractures.

"We think that donepezil can improve cognitive function and increase bone mass, making it a very useful drug for patients with dementia and osteoporosis," said lead author Dr. Tsuyoshi Sato, Associate Professor in the Department of Oral and Maxillofacial Surgery, Saitama Medical University. "From the viewpoint of medical economics, this dual purpose could reduce the cost of treating these diseases."

Bone Mass & Density

Two different kinds of cell control the bone mass and density in our bodies: osteoblasts make bone and osteoclasts absorb it. A molecule called acetylcholine causes osteoclasts to die in vitro. Although an enzyme called acetylcholinesterase breaks this molecule down, the effect of this enzyme on osteoclasts remains unclear.

The most common drug used to treat Alzheimer's disease, donepezil, stops acetylcholinesterase from working, leading to an increase in the amount of acetylcholine in the brain. Recent retrospective clinical studies have suggested that patients being treated with donepezil for Alzheimer's disease have a lower risk of hip fracture, and that risk was dependent on the dose they were taking.

The researchers wanted to understand how donepezil prevents bone degradation. They looked at the drug's activity in vitro using mouse bone marrow cells, and found that more acetylcholinesterase is produced when osteoclasts are being made, which leads to even more osteoclasts being made. Donepezil stops acetylcholinesterase from working, therefore preventing osteoclasts from being made.

Surprising Point

The team also looked at the effect of the drug in a mouse model with bone loss. They found that donepezil increases bone mass in mice by preventing the production of osteoclasts.

"We were surprised to see that donepezil directly inhibits the production of osteoclasts and subsequently increases bone mass in vivo," said Dr. Sato. "This is very surprising point - donepezil directly controls the molecule that is responsible for macrophages becoming osteoclasts."

Previous research has shown that acetylcholinesterase activity increases continuously with age, and may accelerate the risk of bone loss in elderly people. The researchers noted that the concentration of acetylcholinesterase in macrophages was higher when the tissue was inflamed. This suggests that inflammation causes bone to be degraded in part due to acetylcholinesterase production.

"Our findings are very promising and suggest that there is a role for donepezil in increasing bone mass in elderly patients with inflammation and dementia," said Dr. Sato. "There is still work to be done and we look forward to observing the effect of this drug in patients."

The team now plans to work with the Department of Neurology at Saitama Medical University on clinical research. They plan to study whether taking donepezil reduces patients' risk of bone fracture by looking at its effect in a group of patients compared to a control group.

MORE INFORMATION:
"Donepezil prevents RANK-induced bone loss via inhibition of osteoclast differentiation by downregulating acetylcholinesterase" by Sato et al. (doi: 10.1016/j.heliyon.2015.e00013). The article appears in Heliyon (September 2015), published by Elsevier.

Tuesday, August 22, 2017

Is sundowning curable

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

University of Cambridge

arly-evening restlessness and agitation, known as 'sundowning', is common in Alzheimer's. So is fragmented sleep. A major discovery indicates these symptoms are curable.

People with Alzheimer's often have poor biological rhythms, something that is a burden for both patients and their carers. Periods of sleep become shorter and more fragmented, resulting in periods of wakefulness at night and snoozing during the day. They can also become restless and agitated in the late afternoon and early evening, something known as 'sundowning'.

The fly brain is half a millimeter across and contains approximately 100,000 nerve cells (green). The A-beta peptide forms plaques (red) that are linked to nerve cell death and behavioral abnormalities in the flies. Credit: Dr. Stanislav Ott, Department of Genetics, University of Cambridge

Now, scientists from Cambridge have discovered that in fruit flies with Alzheimer's the biological clock is still ticking but has become uncoupled from the sleep-wake cycle it usually regulates. The findings -- published in Disease Models & Mechanisms -- could help develop more effective ways to improve sleep patterns in people with the disease.

Biological clocks go hand in hand with life, and are found in everything from single celled organisms to fruit flies and humans. They are vital because they allow organisms to synchronise their biology to the day-night changes in their environments.

Until now, however, it has been unclear how Alzheimer's disrupts the biological clock. According to Dr Damian Crowther of Cambridge's Department of Genetics, one of the study's authors: "We wanted to know whether people with Alzheimer's disease have a poor behavioural rhythm because they have a clock that's stopped ticking or they have stopped responding to the clock."

The team worked with fruit flies -- a key species for studying Alzheimer's. Evidence suggests that the A-beta peptide, a protein, is behind at least the initial stages of the disease in humans. This has been replicated in fruit flies by introducing the human gene that produces this peptide.

Taking a group of healthy flies and a group with this feature of Alzheimer's, the researchers studied sleep-wake patterns in the flies, and how well their biological clocks were working.

They measured sleep-wake patterns by fitting a small infrared beam, similar to movement sensors in burglar alarms, to the glass tubes housing the flies. When the flies were awake and moving, they broke the beam and these breaks in the beam were counted and recorded.

To study the flies' biological clocks, the researchers attached the protein luciferase -- an enzyme that emits light -- to one of the proteins that forms part of the biological clock. Levels of the protein rise and fall during the night and day, and the glowing protein provided a way of tracing the flies' internal clock.

"This lets us see the brain glowing brighter at night and less during the day, and that's the biological clock shown as a glowing brain. It's beautiful to be able to study first hand in the same organism the molecular working of the clock and the corresponding behaviours," Dr Crowther said.

They found that healthy flies were active during the day and slept at night, whereas those with Alzheimer's sleep and wake randomly. Crucially, however, the diurnal patterns of the luciferase-tagged protein were the same in both healthy and diseased flies, showing that the biological clock still ticks in flies with Alzheimer's.

"Until now, the prevailing view was that Alzheimer's destroyed the biological clock," said Crowther.

"What we have shown in flies with Alzheimer's is that the clock is still ticking but is being ignored by other parts of the brain and body that govern behaviour. If we can understand this, it could help us develop new therapies to tackle sleep disturbances in people with Alzheimer's."

Dr Simon Ridley, Head of Research at Alzheimer's Research UK, who helped to fund the study, said: "Understanding the biology behind distressing symptoms like sleep problems is important to guide the development of new approaches to manage or treat them. This study sheds more light on the how features of Alzheimer's can affect the molecular mechanisms controlling sleep-wake cycles in flies.

"We hope these results can guide further studies in people to ensure that progress is made for the half a million people in the UK with the disease."

Source:

University of Cambridge

Journal Reference:

K.-F. Chen, B. Possidente, D. A. Lomas, D. C. Crowther. The central molecular clock is robust in the face of behavioural arrhythmia in a Drosophila model of Alzheimer's disease. Disease Models & Mechanisms, 2014; DOI:10.1242/dmm.014134

Sunday, August 20, 2017

Celebrate World Alzheimer's Day

Author Susan Berg says "It is everyone’s duty to embrace this day because there is no time to lose when fighting the battle of preventing this terrible disease." Here are some simple things you can do

What do you know about Alzheimer’s disease and related dementias?

How can you decrease your chances of getting these disease?

How can you help someone with Alzheimer’s disease or a related dementia?

This year’s theme is 'Faces of Dementia!'
Yes, there is an urgency for all to learn about these diseases and do what they can to prevent them in themselves. Also legislators need to contacted so more funds can be allocated for research. World Alzheimer’s day, on Sept 21, is the perfect time to do this.

Approximately 5.5 million people in the United States already have Alzheimer’s disease or a related dementia. The number will continue to grow as the baby boomers reach the age of retirement.

What can you do right now to lessen your chances of getting these diseases?

1. Stop smoking! There is nothing positive about smoking. Studies have shown that smoking not only raises your chances of developing dementia, but it also increases your chances of getting other diseases.

2. Eat a healthy diet. Research suggests that the Mediterranean diet staves off the onset of dementia

3. Keep mentally active. Again studies have shown this, to be a way to delay the onset of dementia.

4. Keep physically active. Research indicates that moderate exercise at least a half an hour three times a week is another way to keep dementia from affecting you.

How can you help others?

Donate to the Alzheimer’s Association. Give your time and/ or money. Help with special events. Organize fund raisers.

Susan Berg has written a book called, Adorable Photographs of Our Baby, for those with dementia, their caregivers, and interested professionals.
She is donating money to the Alzheimer’s Association for each book she sells. She is passionate about educating others on these diseases. Visit her blog at http://dementiaviews.blogspot.com.

You or someone you know could develop symptoms tomorrow. The cost of caring for those with Alzheimer’s disease or a related dementia is expensive monetarily, physically, emotionally, and psychologically.

So please acknowledge World Alzheimer’s Day, September 21

Friday, August 18, 2017

Solving the Puzzle of Alzheimer’s Disease

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow alzheimersideas on twitter

The Dementia Caregiver's Little Book of Hope [Kindle Edition

Neuroscience News

Summary: A new study reports a compound by the name of AC253 may inhibit amyloid beta.

Source: University of Alberta.

UAlberta scientist seeks to neutralize ‘rogue’ protein believed to be a key player in the development of Alzheimer’s.

Every day tens of thousands of Canadians unwillingly find themselves becoming shadows of their former selves. They grasp onto moments of clarity–fleeting windows of time–before slipping away again into confusion; robbed of memories, talents and their very personalities.

Alzheimer’s is a heart-wrenching disease that directly affects half a million Canadians. There is no cure, let alone treatment to stop progression of the disease. While current answers are few, research at the University of Alberta is spearheading the discovery of new potential therapies for the future.

A study published in the journal Alzheimer’s and Dementia: Translational Research and Clinical Intervention examines if a compound called AC253 can inhibit a “rogue” protein called amyloid. The protein is found in large numbers in the brains of Alzheimer’s patients and is suspected to be a key player in the development of the disease.

“The way I look at it, it’s hard to ignore the biggest player on the stage, which is the amyloid protein. Whatever treatment you develop, it’s got to address that player,” says Jack Jhamandas, Professor of Neurology in the Faculty of Medicine & Dentistry at the University of Alberta and senior author of the study. “In our previous work we have shown that there are certain drug compounds that can protect nerve cells from amyloid toxicity. One of these is a compound we call AC253. It sounds like an Air Canada flight. I hope this one is on time and takes us to our destination!”

The team, comprised of postdoctoral fellows and research associates Rania Soudy, Aarti Patel and Wen Fu, tested AC253 on mice bred by David Westaway (a University of Alberta collaborator) to develop Alzheimer’s. Mice were treated with a continuous infusion of AC253 for five months, beginning at three months of age before development of the disease.

“We found at eight months, when these mice typically have a lot of amyloid in the brain and have a lot of difficulty in memory and learning tasks, that they actually improved their memory and learning,” says Jhamandas, also a member of the U of A’s Neuroscience and Mental Health Institute.

As part of the study, the team of local and international researchers also developed and tested a more efficient method of getting the compound into the brain. Given an injection three times a week for 10 weeks of AC253 with a slightly modified structure, they again found there was an improvement in memory and learning performance. In addition, the researchers noted there was a lower amount of amyloid in the brains of mice treated with the compound compared to mice that did not get the drug, and that they exhibited reduced inflammation of the brain.

The team is now planning additional studies to examine optimal dosage and methods of further improving the compound to increase its effectiveness in the brain. Much more work is needed before the research can move to human trials. Image is for illustrative purposes only.

Despite the long path still ahead, Jhamandas believes the findings offer both hope and a new way forward to unlock the Alzheimer’s enigma.

“Alzheimer’s is a complex disease. Not for a moment do I believe that the solution is going to be a simple one, but maybe it will be a combination of solutions.”

“We can’t build nursing homes and care facilities fast enough because of an aging population. And that tsunami, the silver tsunami, is coming if not already here,” adds Jhamandas. “At a human level, if you can keep someone home instead of institutionalized, even for a year, what does it mean to them? It means the world to them and their families.”

ABOUT THIS ALZHEIMER’S DISEASE RESEARCH ARTICLE

Funding: Funding provided by Canadian Institutes of Health Research, Alberta Innovates, Alberta Prion Research Institute, Alzheimer Society of Alberta, University Hospital Foundation.

Source: Ross Neitz – University of Alberta
Image Source: NeuroscienceNews.com image is in the public domain.
Original Research: Full open access research for “Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease” by Rania Soudy1, Aarti Patel, Wen Fu, Kamaljit Kaur, David MacTavish, David Westaway, Rachel Davey, Jeffrey Zajac, and Jack Jhamandas in Alzheimer’s and Dementia. Published online December 9 2016 doi:10.1016/j.trci.2016.11.005

CITE THIS NEUROSCIENCENEWS.COM ARTICLE

University of Alberta “Solving the Puzzle of Alzheimer’s Disease.” NeuroscienceNews. NeuroscienceNews, 16 February 2017.
.

Abstract

Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease

Introduction
Amylin receptor serves as a portal for the expression of deleterious effects of amyloid β-protein (Aβ), a key pathologic hallmark of Alzheimer’s disease. Previously, we showed that AC253, an amylin receptor antagonist, is neuroprotective against Aβ toxicity in vitro and abrogates Aβ-induced impairment of hippocampal long-term potentiation.

Methods
Amyloid precursor protein–overexpressing TgCRND8 mice received intracerebroventricularly AC253 for 5 months. New cyclized peptide cAC253 was synthesized and administered intraperitoneally three times a week for 10 weeks in the same mouse model. Cognitive functions were monitored, and pathologic changes were quantified biochemically and immunohistochemically.

Results
AC253, when administered intracerebroventricularly, improves spatial memory and learning, increases synaptic integrity, reduces microglial activation without discernible adverse effects in TgCRND8 mice. cAC253 demonstrates superior brain permeability, better proteolytic stability, and enhanced binding affinity to brain amylin receptors after a single intraperitoneal injection. Furthermore, cAC253 administered intraperitoneally also demonstrates improvement in spatial memory in TgCRND8 mice.

Discussion
Amylin receptor is a therapeutic target for Alzheimer’s disease and represents a disease-modifying therapy for this condition.

“Cyclic AC253, a novel amylin receptor antagonist, improves cognitive deficits in a mouse model of Alzheimer’s disease” by Rania Soudy1, Aarti Patel, Wen Fu, Kamaljit Kaur, David MacTavish, David Westaway, Rachel Davey, Jeffrey Zajac, and Jack Jhamandas in Alzheimer’s and Dementia. Published online December 9 2016 doi:10.1016/j.trci.2016.11.005

FEEL FREE TO SHARE THIS NEUROSCIENCE NEWS.

Wednesday, August 16, 2017

Alzheimer's personality and behavior changes

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

ADEAR
n dementia, the brain loses a number of abilities. This can change a person's personality and behavior. Use this tip sheet's suggestions to better understand them.

Changes in the way people act can be one of the biggest challenges in caring for people with Alzheimer's.

There is much you can do to smooth the journey.

COMMON CHANGES IN PERSONALITY AND BEHAVIOR

Common personality and behavior changes you may see include:

Getting upset, worried, and angry more easily
Acting depressed or not interested in things
Hiding things or believing other people are hiding things
Imagining things that aren't there
Wandering away from home
Pacing a lot
Showing unusual sexual behavior
Hitting you or other people
Misunderstanding what he or she sees or hears

You also may notice that the person stops caring about how he or she looks, stops bathing, and wants to wear the same clothes every day.
In addition to changes in the brain, other things may affect how people with
Alzheimer's behave:

Feelings such as sadness, fear, stress, confusion, or anxiety
Health-related problems, including illness, pain, new medications, or lack of sleep
Other physical issues like infections, constipation, hunger or thirst, or problems seeing or hearing
Problems in their surroundings, like too much noise or being in an unfamiliar place

If you don't know what is causing the problem, call the doctor. It could be caused by a physical or medical issue.

KEEP THINGS SIMPLE… AND OTHER TIPS

Caregivers cannot stop Alzheimer's-related changes in personality and behavior, but they can learn to cope with them. Here are some tips:

Keep things simple. Ask or say one thing at a time.
Have a daily routine, so the person knows when certain things will happen.
Reassure the person that he or she is safe and you are there to help.
Focus on his or her feelings rather than words. For example, say, "You seem worried."
Don't argue or try to reason with the person.
Try not to show your frustration or anger. If you get upset, take deep breaths and count to 10. If it's safe,
leave the room for a few minutes.
Use humor when you can.
Give people who pace a lot a safe place to walk.
Try using music, singing, or dancing to distract the person.
Ask for help. For instance, say, "Let's set the table" or "I need help folding the clothes."

Talk with the person's doctor about problems like hitting, biting, depression, or hallucinations. Medications are available to treat some behavioral symptoms.

MORE INFORMATION:
For more caregiving tips and other resources:

Read "Caring for a Person with Alzheimer's Disease":
Visit www.nia.nih.gov/alzheimers/topics/caregiving
Call the ADEAR Center toll-free:
1-800-438-4380

SOURCE:

The Alzheimer's Disease Education and Referral (ADEAR) Center is a service of the National Institute on Aging, part of the National Institutes of Health. The Center offers information and publications for families, caregivers, and professionals about Alzheimer's disease and age-related cognitive changes.

Monday, August 14, 2017

Dementia and HS aging

Caregivers, and healthcare professionals,here is some great information

Here is a great dementia resource for caregivers and healthcare professionals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow alzheimersideas on twitter
The Dementia Caregiver's Little Book of Hope [Kindle Edition]

University of Kentucky Sanders-Brown Center on Aging

3 important dementia studies focus on HS-AGING. It's a type of dementia almost as common as Alzheimer's in the 85+ group. Yet few people have heard of it. Why? What makes it different?

In those who live to a very advanced age (beyond the age of 85) HS-AGING (hippocampal sclerosis in the elderly) is almost as prevalent as Alzheimer's. Remarkably, HS-Aging appears to be a completely separate disease from Alzheimer's, although it is almost always diagnosed as Alzheimer's disease while people are alive.

Three important papers authored by Dr. Peter Nelson and others at the University of Kentucky Sanders-Brown Center on Aging, explore the neuropathology behind this little-understood brain disease.

HS-AGING, much like Alzheimer's disease, causes symptoms of dementia, such as cognitive decline and impaired memory. Although Alzheimer's disease is probably the most recognized cause of dementia, HS-AGING also causes serious cognitive impairment in many older adults.

Overview of 3 New Studies on HS-AGING:

The first paper, published in the Journal of Alzheimer's Disease, draws from a very large sample population and shows that presently, around 20% of all dementia cases are diagnosed as HS-AGING at autopsy, although almost none are given that diagnosis during life. That means that the presence of this disease is currently almost unknown by the health care providers who are seeing patients.
A second study, "Arteriolosclerosis that affects multiple brain regions," appears in a recent issue of the journal Brain, and looks at small blood vessels in patients with HS-Aging and describes a specific change, called "arteriolosclerosis," which is present in patients with HS-Aging. This small blood vessel change may provide a new therapeutic target to alter the progression of the disease.
Finally, the third paper, "Hippocampal sclerosis of aging, a prevalent and high morbidity brain disease," appears in Acta Neuropathologica and offers an overview of HS-AGING for patients and researchers. This paper reviews the relevant scientific literature and also presses home the point that HS-AGING is a very common disease that exerts a strongly adverse impact on public health.

It is important for physicians and scientists to understand the unique pathology of HS-AGING, and to be able to differentiate it from other diseases, as it is only by making an accurate diagnosis that clinicians can hope to treat people who present with signs of cognitive decline. These current studies represent a leap forward in the knowledge base about HS-AGING, and represent potential new paths to explore for diagnosis and treatment of this serious, but under-appreciated brain disease.

In people over 95, a type of dementia called HS-Aging is about as common as Alzheimer's. Yet few people have heard of it. Why? What makes it different?

What is HS-Aging?

HS-Aging stands for "Hippocampal Sclerosis in Aging People".

Alzheimer's and HS-Aging are types of dementia. In people over 95, their prevalence is about equal.

HS-Aging is Not Well Known. Everyone Has Heard of Alzheimer's. Why?

There are hundreds of types of dementia. In people aged 65 to 95, 60% of dementia cases are Alzheimer's. That is why Alzheimer's is so well-known.

At age 95, the balance shifts and HS-Aging becomes about as common as Alzheimer's.

Few people have heard of HS-Aging. The main reason is because it is often mis-diagnosed as Alzheimer's. Why?

When dementia is seen in the elderly, the default diagnosis is Alzheimer's. This is caused by many factors, among them:

Patients often do not want to go through extensive testing for a variety of reasons.
There is no simple test. The differences between dementias can be subtle. Therefore, distinguishing between dementias is often technically challenging.
Cost comes into play. For example, F18 dementia scans can run thousands of dollars. Therefore, many a diagnosis is made based on incomplete information.

With these realities, it is common for a diagnosis to default to the most common dementia, which is Alzheimer's.

As a result, people with dementias such as HS-Aging often live out their lives thinking they have Alzheimer's.

How does HS-Aging differ from Alzheimer's?

Alzheimer's and HS-Aging both damage the hippocampus. It seems that HS-Aging hits harder than Alzheimer's, causing greater disturbances to memory.

HS-Aging describes a brain under attack from a protein called TDP-43. It causes sclerosis, or the hardening of tissues. In the case of HS-Aging, TDP-43 proteins harden brain tissue in the hippocampus (sometimes called the memory-processing center), causing the loss of a large number of crucial brain cells. It is called Hippocampal Sclerosis because the brain's hippocampus is the focus of the attack.

Alzheimer's, on the other hand, is an attack on the brain by plaques (made from beta-amyloid) and tangles (made of tau proteins). Researchers speculate that the plaques clump together and "choke" brain cells, while the tangles strangle them from within.

How does HS-Aging differ from regular HS?

Regular Hippocampal Sclerosis (HS) occurs in younger people where brain tissue hardening is associated with epilepsy. HS-Aging is a similar hardening, but it occurs in the elderly with different consequences. It is caused by a long life of physical wear-and-tear on the brain, similar to vascular dementia. As a matter of fact, once people hit 95, the combined occurrences of HS-Aging PLUS vascular dementia actually outstrip Alzheimer's.

Why does the type of dementia matter?

As explained above, the biochemistry of each dementia differs significantly. This implies different medications are required to fight the chemicals causing the dementia. A person's response to medicines and supplements will be entirely different, depending on the disease.

Importantly, new F18 imaging techniques have recently been introduced that let doctors see if a person with dementia has the plaques associated with Alzheimer's. Using this technique helps doctors tell the difference between Alzheimer's and HS-Aging. This is particularly crucial in the world of clinical trials, where participants must closely match the experimental drugs they are testing.

CTE Research Leading to Rapid Improvements in HS-Aging Treatments

When we talk about dementia in aging athletes, it is usually the type of dementia called CTE (Chronic Traumatic Encephalopathy). Recent studies showed athletes in contact sports like football are 19 times more likely than average to develop dementia. As a result, there has been a huge burst of research on CTE treatment.

CTE treatment has a lot in common with HS-Aging treatment. With the new attention both of these dementias are now receiving, there is good reason to hope for effective new treatments in the immediate future.

MORE INFORMATION:
Study #1 above was done with the collaboration of the National Alzheimer's Coordinating Center (or "NACC"; the first author of this study, Willa Brenowitz, is based in Washington state and works with NACC), enabling Nelson and colleagues to incorporate data from dozens of federally funded Alzheimer's Disease Centers around the country. These centers are funded by the National Institute on Aging, part of the National Institutes of Health. The research was supported by NIA grant numbers U01 AG016976 and P30 AG028383.

Study #2 above was based on analyses that were boosted through collaboration with the larger NACC-based dataset. Further, the first author, Dr. Janna Neltner, provided critical expertise in digital pathologic measurement of the brain.

SOURCE:
University of Kentucky Sanders-Brown Center on Aging