Social Media

After having a lot of problems recently, I have decided to close down some of my social media links

This is because I am struggling to cope with it all these days It's very sad, but I think it's time to step back and take things easy

Part of the problem is that I have noticed a rise in political and racial hatred etc, and I want nothing to do with this sort of thing.

Life is too short to get involved with something I have little or no control over, so I have taken the easy route out of it

Many people have complained about the rise in hatred on these sites, so I guess it's time to say goodbye to many people.

I am sure that anyone wishing to contact me, can still do do using other methods in the future

Ken

Social Media

After having a lot of problems recently, I have decided to close down some of my social media links

This is because I am struggling to cope with it all these days It's very sad, but I think it's time to step back and take things easy

I am also getting tired struggling a little with my health  and confess my eyesight etc is not what is used to be

Part of the problem is that I have noticed a rise in political and racial hatred etc, and I want nothing to do with this sort of thing.

Life is too short to get involved with something I have little or no control over, so I have taken the easy route out of it

Many people have complained about the rise in hatred on these sites, so I guess it's time to say goodbye to many people.

I am sure that anyone wishing to contact me, can still do do using other methods in the future

Ken

Lewy Body Dementia and Alzheimer's

DEAR MAYO CLINIC: What’s the difference between Lewy body dementia and Alzheimer’s? How is Lewy body dementia diagnosed?

ANSWER: Doctors diagnose Lewy body dementia based on the range of symptoms a person shows. Generally, the diagnosis requires an ongoing decline in thinking skills, along with two of the following: visual hallucinations, Parkinsonism or fluctuating alertness. In addition, people who have Lewy body dementia also may experience a sleep condition known as REM sleep behavior disorder, in which people act out their dreams while they sleep. They also may have instability in their blood pressure and heart rate, and the body may have difficulty controlling body temperature and sweating.

A brain disease that gets worse over time, Lewy body dementia is caused by an abnormal protein, called synuclein, which is deposited in certain nerve cells and nerve processes. These deposits are called Lewy bodies — named after the physician who first identified them. In Lewy body dementia, Lewy bodies are found in the deep structures of the brain that control movement, as well as in the middle and outer structures involved in emotion, behavior, judgment and awareness.

Many patients with Lewy body dementia also have overlapping Alzheimer’s disease. About half of Lewy body patients have significant Alzheimer’s disease, as well. Thus, it is not surprising that those diagnosed with Lewy body dementia have symptoms associated with Alzheimer disease, such as memory loss and naming difficulty. However, when doctors who have expertise and experience with the disease make a Lewy body dementia diagnosis, that diagnosis is often correct — as confirmed later during an autopsy. An accurate diagnosis is important, because Lewy body dementia responds differently than Alzheimer’s disease to commonly prescribed dementia medications.

Lewy body dementia usually progresses gradually over several years, but the way it progresses can vary significantly from person to person. For example, Lewy body dementia may begin with signs of dementia, and Parkinsonism appears later. Or the disease may start with movement difficulties, and signs of dementia don’t emerge for some time. Most people with Lewy body dementia experience the onset of Parkinsonism and dementia within one year. As Lewy body dementia progresses, all symptoms usually become more severe.

Hallucinations occur early in Lewy body dementia but only after about four years in Alzheimer’s disease. If a person acts out dreams, that is strong evidence that he or she has synuclein protein in the brain. This protein is found only in Lewy body dementia, Parkinson’s disease and a rare disease called multiple system atrophy. Acting out one’s dreams is a feature in all of these diseases.

Lewy body dementia is a complex disease, and it can be difficult to control. Currently, there’s no cure. But, when treatment is carefully managed, symptoms may be reduced, so they have less effect on a person’s daily functioning and quality of life.

Some people diagnosed with Lewy body dementia respond positively to medications called cholinesterase inhibitors. They boost the level of a chemical messenger in the brain called acetylcholine that’s important for memory and other cognitive functions. These drugs may help improve alertness and reduce hallucinations and signs of dementia.

Other medications are available to help decrease the Parkinsonism, hallucinations and other Lewy body dementia symptoms. These medications must be closely monitored by a health care provider. In people who have Lewy body dementia, medications to improve motor function may make symptoms such as hallucinations worse, and medications used to combat dementia may increase Parkinsonism.

Because Lewy body dementia treatment needs to be managed skillfully to obtain the most effective results, people who have this disease should be monitored by a physician with expertise and experience with Lewy body dementia — usually a neurologist or a neuropsychiatrist. — Neill Graff-Radford, M.D., Neurology, Mayo Clinic, Jacksonville, Fla.

(Mayo Clinic Q & A is an educational resource and doesn’t replace regular medical care. E-mail a question to MayoClinicQ&A@mayo.edu. For more information, visit www.mayoclinic.org.)

(c) 2017 MAYO FOUNDATION FOR MEDICAL EDUCATION AND RESEARCH. ALL RIGHTS RESERVED. DISTRIBUTED BY TRIBUNE CONTENT AGENCY, LLC.

  

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Exercising may improve the memory

Exercising Twice a Week may Improve Memory of Mild Cognitive Impaired Patients

Pareesh Phulkar Jan 17, 2018

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New guidelines released by American Academy of Neurology (AAN) reports that exercising twice a week may improve cognitive abilities and memory of patients suffering from mild cognitive impairment (MCI).

MCI causes a slight but noticeable and measurable decline in cognitive abilities, including memory and thinking skills. A person with MCI can be at high risk of developing Alzheimer’s or dementia. This a medical condition is common with aging. People with MCI are unable to complete complex tasks or have difficulty understanding information they have read, whereas people with dementia have trouble with daily tasks, such as dressing, bathing and eating. The guidelines are recommended by the Alzheimer’s Association, which is an update to the AAN’s previous guideline on mild cognitive impairment. It was published on December 27, 2017, in Neurology, the medical journal of the American Academy of Neurology.

“It’s exciting that exercise may help improve memory at this stage, as it’s something most people can do and of course it has overall health benefits,” said lead author Ronald C. Petersen, MD, PhD, of the Mayo Clinic in Rochester, Minn and a Fellow of the American Academy of Neurology. “Because MCI may progress to dementia, it is particularly important that MCI is diagnosed early.”

There are no FDA approved medications for the treatment of MCI. Moreover, there are no high-quality, long-term studies that suggest drugs or dietary changes can improve thinking ability or delay memory problems in people with MCI. Guidelines recommends that people suffering from MCI should exercise regularly as part of managing their symptoms. Although long-term studies have not been conducted for this, six-month studies suggest twice-weekly workouts may improve memory.

According to Medical Devices report published by Coherent Market Insights, medical devices can be used to monitor the activities of patients after exercising and before exercising, which can reveal if exercising twice a week according to the guidelines is lowering the symptoms in patients suffering from MCI. Physicians may recommend cognitive training for people with MCI. It may be beneficial in improving measures of cognitive function. More than 37% of people at the age of 85 and older are suffering from MCI.

Alzheimer'sDementiaNeurology

Zonisamide may help those with DLB

Zonisamide may help those with dementia with Lewy bodies

A drug used to treat seizures may effectively treat the movement symptoms in people with dementia with Lewy bodies without causing additional psychiatric symptoms…

Researchers have found that a drug used to treat seizures may effectively treat the movement symptoms in people with dementia with Lewy bodies without causing additional psychiatric symptoms when combined with the Parkinson’s drug levodopa.

Adding zonisamide to the current dose of levodopa was safe and improved movement symptoms

Dementia with Lewy bodies can include movement problems like stiffness, tremor and shuffling of feet. Because it has many symptoms in common with Alzheimer’s and Parkinson’s diseases, it can be difficult to diagnose and treat.

A drug commonly used to treat movement symptoms in Parkinson’s, levodopa, may worsen psychiatric symptoms in those with dementia with Lewy bodies, especially when higher doses are given as the effects of levodopa start to wane.

“We found that adding zonisamide to the current dose of levodopa was safe and improved movement symptoms in those with dementia with Lewy bodies without magnifying hallucinations, delusions or agitation,” said study author Dr Miho Murata, of the National Center of Neurology and Psychiatry in Tokyo, Japan.

For the study, researchers followed 158 people diagnosed with early dementia with Lewy bodies who had been living with the disease for an average of one-and-a-half years. Participants were given either placebo, 25 milligrams of zonisamide daily or 50 milligrams of zonisamide daily. This was in addition to already taking other medications for the disease. Their movement symptoms were measured as were their thinking abilities, behaviour and psychological symptoms. At the beginning of the study, the participants had an average score of 32 on the movement test, on a scale of zero to 108.

Researchers found that after 12 weeks, those taking 50 milligrams a day of zonisamide in conjunction with levodopa had improved more than four points on the movement scale compared to those who took a placebo. Researchers found no worsening of the psychological symptoms.

“There is an urgent need for new treatments for dementia with Lewy bodies,” said Dr Linda A. Hershey, of the University of Oklahoma Health Sciences Center in Oklahoma City, Okla. “The successful execution of this trial is a major accomplishment, which provides evidence that future trials are warranted.”

One limitation of the study was the small number of participants. More studies are needed to investigate the effectiveness of zonisamide in larger populations.

The study has been published in Neurology.

Bronchiectasis and Autoimmune System

Bronchiectasis May Trigger Autoimmune Inflammatory Disease, Study Suggests

January 9, 2018

by Magdalena Kegel

In News.

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Bronchiectasis is commonly found in patients with autoimmune conditions, causing blood vessel inflammation, a recent study found.

Moreover, the presence of bronchiectasis in these patients is linked to specific disease features, raising the possibility that these autoimmune diseases may be triggered by respiratory tract conditions, researchers argued in the journal Seminars in Arthritis and Rheumatism.

The study, “Bronchiectasis is highly prevalent in anti-MPO ANCA-associated vasculitis and is associated with a distinct disease presentation,” was performed by researchers at Nantes University Hospital and INSERM in France.

Granulomatosis with polyangiitis (GPA) or microscopic polyangiitis (MPA) are two forms of blood vessel inflammation linked to so-called ANCA autoantibodies. These antibodies target two proteins known as PR3 and MPO, ultimately resulting in organ damage.

Patients with GPA often have respiratory problems before apparent blood vessel inflammation, but MPA-affected patients also develop respiratory disease.

Earlier studies suggest that many patients with ANCA vasculitis have bronchiectasis, but it is not yet clear how presence of the lung condition impacts the autoimmune disease.

To explore this, researchers recruited 58 Caucasian patients with ANCA vasculitis; 28 had GPA-type disease and 30 had MPA.

Among the patients, 67.2 percent had anti-MPO antibodies and 32.8 percent had anti-PR3 antibodies.

Twenty-two of the patients (37.9 percent) had bronchiectasis. All of these affected patients had anti-MPO ANCA antibodies. In the group with anti-MPO antibodies, 56.4 percent had imaging evidence of bronchiectasis and another four had bronchiectasis symptoms.

Patients with lung disease more often had symptoms of peripheral nervous system and movement impairment compared to those without bronchiectasis. On the other hand, they were less likely to have kidney disease. In fact, they had better kidney function than patients without bronchiectasis, despite being older.

Statistical analysis revealed that bronchiectasis was linked to anti-MPO antibodies, female sex and age at the time of ANCA vasculitis diagnosis.

Patients with bronchiectasis, however, did have a similar disease course and risk of severe lung infection as those without the condition. Survival rates also were not dependent on bronchiectasis.

The data indicates that the autoimmune processes in ANCA vasculitis may start in the respiratory system, at least in a subset of patients, researchers said.

“This study shows that bronchiectasis is a highly prevalent pre-existing respiratory condition in Caucasian patients with anti-MPO AAV [ANCA-associated vasculitis]. This subset of patients exhibits a distinct presentation.” the team wrote.

More studies are now needed to explore how bronchiectasis may impact disease processes in ANCA vasculitis patients, and “whether the respiratory tract could be the site of initiation of anti-MPO auto-immunity” the researchers concluded.

Brain Donation Process

Newcastle Brain Tissue Resource (NBTR)

• The Donation Process
• For The Public
• For Researchers
• Ethics and Regulation
• Contact us

The NBTR is a partnership between the Medical Research Council, local NHS trusts and Newcastle University. It has contributed to important medical advances such as new treatments for Alzheimer's disease and the identification of a common type of dementia in older people called Dementia with Lewy Bodies.

Brain Donations

The donation of brain tissue to research is an invaluable source of help. Studies using human brain tissue are essential in increasing our understanding of brain ageing and related diseases and are the best way for us to search for more effective diagnoses and treatments.

Even though progress in research towards finding causes of and treatments for a wide variety of diseases and disorders is a concern for all of us, few people realise that in many cases it cannot be achieved without human tissue.

Research projects are currently running with the help of volunteers diagnosed with diseases such as Alzheimer's disease, Parkinson's disease, Lewy Body dementia and Stroke. Studying tissue donated by sufferers of these diseases helps us to discover what brain changes take place during the course of the disease and increases our overall understanding.

Who can donate tissue?

Each individual brain tissue donation is very important to us. At present we are only able to accept donations of affected tissue from people who are part of the University's study programmes and are extremely grateful to those patients and families who continue to facilitate our research in this way.

Brain tissue from donors without memory impairment is also a very important gift. Research progress already made would not have been possible without healthy tissue which is used to establish the brain changes which occur in normal ageing rather than as a result of disease. We would like to encourage people without neurological difficulties to consider donating brain tissue at the time of their death and have a register to which prospective normal donors aged 65 years and over may wish to add their name.

For more information please contact our nurse liaison team who will be happy to provide you with more information:

• Email: nbtr@ncl.ac.uk or telephone our research nurses:
• Debbie Lett on 0191 208 1231
• Susan Richardson on 0191 208 1229