2016 Alzheimer’s Disease Facts and Figures

April 20, 2016 Categories AG Scientific Blog
Alzheimers

2016 Alzheimer’s Disease Facts and Figures

The information below was made available by the Alzheimer’s Association in the United States. They highlight the 2016 Alzheimer facts and figures and how it affects the people in our nation financially and personally, as caregivers, providers, patients, and victims. There is also information on AD Milestones as well as some details on current research.

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In the United States

As the inforgraphic shows, every 66 seconds someone in the U.S. develops Alzheimer’s Disease (AD). With more than 5 million Americans living with AD, 1 in 3 of seniors will die with AD or another dementia. 18.1 billion hours of unpaid care is estimated to have been provided by more than 15 million caregivers.

Major Milestones as reported by Alz.org:

2011

President Obama signs
National Alzheimer’s Project Act (NAPA) into law

First-ever framework for a national strategic plan to address AD and coordinate research, care, and support programs was created in the USA.

2013

International Genomics of Alzheimer’s Project (IGAP)
researchers identify new genetic risk factors for
Alzheimer’s disease

Researchers from around the world collaborated to make a meta-analysis of genome-wide association studies that identify genetic variations linked with an increase for AD. It showed there are 20 genetic variations associated with AD risk, 11 of them not having been linked to AD previously, and some newly identified genetic variations are thought to be immune system specific, adding to mounting evidence of a role for the immune system in AD.

Targets for future drugs


Developments by researchers over the last 30 years, have led to remarkable progress in understanding healthy brain function and issues that contribute to Alzheimer’s disease. Listed below are examples of promising targets for next-generation drug therapies being investigated in current research studies:

  • Beta-amyloid: the chief component of plaques, a hallmark of Alzheimer’s brain abnormality. Scientists have an understanding of how this protein fragment is clipped from its parent compound amyloid precursor protein (APP) by two enzymes — beta-secretase and gamma-secretase. Researchers are developing medications aimed at every point in amyloid processing including: blocking activity of beta-secretase enzyme; preventing the beta-amyloid fragments from clumping into plaques; and even using antibodies against beta-amyloid to clear it from the brain.

    C
    urrent drug in research that targets beta-amyloid: Solanezumab
    Solanezumab, a monoclonal antibody, is designed to lower the level of beta-amyloid in the brain. These antibodies bind to beta-amyloid and prevent the formation of plaques. Solanezumab may also help carry excess beta-amyloid away from the brain. Several studies of solanezumab are under way with the goal determining if it improves participants’ cognition (thinking and memory) and functioning. Some participants will undergo a brain scan called positron emission tomography (PET) to determine levels of beta-amyloid in the brain. (Drug is still in research & not available to the public.)
 Beta-amyloid Protein and Alzheimer’s (approx 13 min.)
  • Beta-secretase (BACE), one of the enzymes that clips APP, makes it possible for beta-amyloid to form. Therapies that interrupt this process might reduce the amount of beta-amyloid in the brain, ultimately intervening in the development of Alzheimer’s disease (AD).

    Current drug in research that targets beta-secretase: MK-8931

    MK-8931 is a BACE inhibitor — it stops the ability of the beta-secretase enzyme to make beta-amyloid. At the Alzheimer’s Association International Conference® 2013 (AAIC®), researchers reported that the drug significantly lowered beta-amyloid levels in people with mild-to-moderate Alzheimer’s Disease. MK-8931 is being tested in two phase 3 clinical trials.
    (Drug is still in research; not available to the public.)
  • Tau protein is the chief component of tangles,  and it is the other hallmark brain abnormality of Alzheimer’s. The Tau protein helps maintain the structure of a neuron, including the tiny tube-like structures “microtubules” that deliver nutrients throughout the neuron. Researchers are searching mechanisms to prevent tau protein from collapsing and twisting into tangles, a process that destroys microtubules and, ultimately, the neuron itself.

    Current drug in research that targets tau protein: AADvac1

    AADvac1 is a vaccine that makes the body’s immune system attack an abnormal form of tau protein that destabilizes the structure of neurons. If it is successful, it has the potential to help stop the progression of Alzheimer’s disease. Researchers at AAIC 2015, reported that AADvac1 was safe and well-tolerated by participants in a phase 1 clinical trial. (Drug is still in research & is not available to the public.)
  • Inflammation is a key in Alzheimer’s brain abnormality. Both beta-amyloid plaques and the tau tangles cause an immune response in the brain. Microglia, cells that act as the first form of immune defense in the brain, help clear beta-amyloid in the brain. However, they may become overactive in the presence of beta-amyloid and produce compounds that damage nearby cells.

    C
    urrent drug in research that targets inflammation: CSP-1103
    CSP-1103 is a microglial modulator; it aims to reduce inflammation in the brain. Researchers at AAIC 2013 presented the results of a 90-week trial in which people who had mild cognitive impairment (MCI) were given CSP-1103. Preliminary studies showed that CSP-1103 prevented beta-amyloid from being deposited on neurons, preventing plaque formation. It reduced problems with thinking and memory (cognition). Cognitive test results of people who had participated for at least 64 weeks showed statistically significant improvements in participants’ cognitive abilities. (Drug is still in research; not available to the public.)

     Inflammation, the Immune System and Alzheimer’s (approx 30 min.)
  • Insulin resistance in the brain is another common feature of Alzheimer’s disease. For reasons not completely know to researchers, the brain becomes resistant to the normal effects of insulin, which includes the conversion of glucose to energy that brain cells can use to fuel cell functioning. There is some research suggesting that beta-amyloid decreases the body’s ability to use insulin. Other research have reported reduced levels of insulin in the brain.

    C
    urrent drug in research that targets insulin resistance: Intranasal insulin
    Intranasal insulin is a therapy drug. It is being tested in multiple studies for its effects on memory, thinking and daily functioning in people with MCI and mild-to-moderate Alzheimer’s disease. There is growing evidence that insulin plays a big role in keeping the brain healthy. Intranasal administration of insulin might help by increasing insulin signaling in the brain.(Drug is still in research; not available to the public.)
 Insulin and Alzheimer’s (approx 22 min.)

Below is additional information on the facts and figures of AD in America.Page2

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To download these images, you can go to www.alz.org

For a fuller 2016 Alzheimer’s Disease Facts and Figures report, please click on the resource below. (via www.alz.org)

2016 alzheimer

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