One step closer to a diagnosis for Alzheimer’s

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Even if you suspected that someone close to you has Alzheimer’s disease, getting a diagnosis isn’t easy. But with the right treatment and support, as well as by focusing on what the person continues to be able to do, you both can still look forward to enjoying many happy times together.

And remember, the changes you’ll see in your loved one will probably be very gradual. These steps can help you cope with those changes, as well as help you plan for what the future may bring. This way, every day can be lived to its fullest.

  • Try to remind yourself that you’ll experience many different feelings and that they’re normal reactions to having someone close to you diagnosed with Alzheimer’s disease.
  • Don’t keep it to yourself. Telling friends or family about the news can bring forth the support you need, and brings you one step closer to accepting the diagnosis.
  • Learn as much as you can about the disease so that you know what to expect – and can plan for the future accordingly.
  • Look at all the options for treating Alzheimer’s disease and discuss them with a doctor, pharmacist or other healthcare professional.
  • Be aware that the disease affects a person’s abilities, so be ready to help out as needed and offer support.
  • Plan for the future – but live each day. By enjoying every moment, you’ll make the most of the time you have with your loved one, and that benefits you both.
  • Learn to use available resources, such as the information and support offered by the Alzheimer Society of Canada.

There is no single test that can show whether a person has Alzheimer’s. While physicians can almost always determine if a person has dementia, it may be difficult to determine the exact cause. Diagnosing Alzheimer’s requires careful medical evaluation, including:

  • A thorough medical history
  • Mental status testing
  • A physical and neurological exam
  • Tests (such as blood tests and brain imaging) to rule out other causes of dementia-like symptoms

Having trouble with memory does not mean you have Alzheimer’s. Many health issues can cause problems with memory and thinking. When dementia-like symptoms are caused by treatable conditions — such as depression, drug interactions, thyroid problems, excess use of alcohol or certain vitamin deficiencies — they may be reversed.

One step closer Jan 2012

Researchers believe they are closer to curtailing the rise in Alzheimer’s disease (AD) with early and accurate diagnostic tests and treatments.

Developments were unveiled at Neuroscience 2012, the annual meeting of the Society for Neuroscience (the world’s largest source of emerging news about brain science and health). These included medical imaging, molecular analysis of neurological diseases and the development of treatments using mouse models.

Scientists at the meeting presented a brain imaging ‘probe’ devised to detect the earliest stages of the disease. The probe works by binding to a protein called amyloid, a key feature of Alzheimer’s. Researchers at Northwestern University and the University of Illinois in the United States developed the probe using an antibody that binds to amyloid, which is known to clump together in the brain and become toxic during Alzheimer’s. The researchers then combined this antibody with magnetic nanoparticles that show up during magnetic resonance imaging (MRI) scans.

Alzheimers brain NASA 500(3)

Current brain scanning techniques only detect amyloid in the brain once it has formed into large, sticky plaques, but the researchers hope their new probe will help detect the toxic form of amyloid before these plaques have formed, in order to identify people with Alzheimer’s at a much earlier stage. The scientists aim to develop a way of delivering the probe – which has so far been tested in the lab and in rodents – using a nasal spray.

Other interesting findings to emerge at the meeting included: revealing how changes in brain function can be detected by positron emission tomography (PET) scans, which might one day be used to identify people at risk of developing the disease; and a new drug that targets biochemical changes in proteins, which has so far improved symptoms and increased survival in a mouse model with AD – although just how it works is not yet known.

Also, a new mouse model for the disease has given researchers more control over an Alzheimer’s-related protein in mice, which could lead to better research on effective treatments.

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There are an estimated 35.6 million people with Alzheimer’s or dementia worldwide. This number is expected to nearly double every 20 years, to an estimated 65.7 million in 2030, and rise to 115.4 million in 2050. Much of the increase will be in developing countries. Already, 58 % of people with dementia live in developing countries, but by 2050 this will rise to 71 %. The fastest growth in the elderly population is taking place in China, India and their south Asian and western Pacific neighbours.

Experiments on mouse models of Alzheimer’s disease (AD) suggest that therapy with male sex hormones might slow its progression. The findings, reported in the December 20 issue of The Journal of Neuroscience, provide new insight into the relationship between testosterone loss and AD, which affects 4.5 million Americans.

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Senior author Christian Pike, PhD, of the University of Southern California (USC), with colleagues at USC and the University of California, Irvine, sought to better understand the role hormones play in aging and disease. Recent studies had already established a link between testosterone loss in men and AD due to natural aging.

The research team established a connection between low testosterone and elevated beta-amyloid (A), a protein that accumulates abnormally in AD patients. This finding, they say, suggests that testosterone depletion in aging men may be a risk factor for AD by promoting accumulation of A in the brain. Testosterone, the primary male sex hormone, is one in a group of related steroid hormones referred to as androgens. Recent studies suggest that androgens may lower A levels.

“This study raises the possibility that androgen replacement treatment might lower the risk for Alzheimer’s, but this is far from proven,” says Sam Gandy, MD, PhD, chair of the Alzheimer’s Association’s Medical and Scientific Advisory Council and director of the Farber Institute for Neurosciences at Thomas Jefferson University. “Because testosterone is rapidly converted to estrogen after entry into neurons, the new data are logical, and they dovetail well with historical data”

Researchers may be one step closer to diagnosing Alzheimer’s disease while the patient is still alive, increasing the opportunity for treatment sooner.

A positive identification is typically not done until after death, when an autopsy can be conducted. While a patient is alive a series of tests may be given to determine brain decline, a less exact method of diagnosis.

For the first time, researchers, using clinical-grade magnetic resonance imaging scans (MRIs), have located Alzheimer’s-like plaque in rabbits.

John Robarts of Ontario’s Roberts Research Institute believes that may have application to humans.

“Although some of the technology used to generate these images was designed specifically for rabbits, this preliminary discovery hints at the promise of using clinical MRI scanners to visualize plaques in people with Alzheimer’s,” he said in a statement.

The MRI scanner was customized with special hardware that generates a microimagine, detecting structures smaller than 50 microns, and which is more sensitive to iron-containing structures.

Previously, amyloid plaques have only been seen or “imaged” using a high powered MRI scanners used only on animals, or with a PET scan using marker chemicals.

This is the first time the amyloid plaques, characteristic of Alzheimer’s disease, have been seen using a conventional MRI.

In the study, rabbits were fed a high-cholesterol diet. That caused the brain to form amyloid plaques. After two years the rabbits’ brains were scanned where researchers saw black spots or signal voids in the brain, particularly the hippocampus where memory is stored.

 

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