Understanding Alzheimer’s Disease: What’s Next? [Infographic]

November 18, 2017
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Alzheimer’s disease can be a harrowing diagnosis to receive because it seems so starkly final. However, a lot is happening on the frontlines of Alzheimer’s research and our understanding of the disease, as well as hope for an eventual cure grow exponentially.

In order to understand the strides that are being made in the research field, it’s important to understand how Alzheimer’s disease attacks the brain and cognitive functions of the person affected.

Alzheimer’s disease causes the following abnormalities in the brain:

-Plaques are the name for microscopic clumps Beta-Amyloid, a protein fragment.

-Tangles are microscopic strands of a protein called tau that become twisted.

-Damage to the communication and connection between brain cells.

-Immune system-caused inflammation

-Brain cell death.

Autosomal Dominant Alzheimer’s Disease (ADAD) or familial alzheimer’s refers to Alzheimer’s disease that is developed genetically from a deterministic gene, meaning that there is a certainty that someone with the gene will develop alzheimer’s at some point in their lives. With ADAD, Alzheimer’s is certain, but there are other genes that are ‘risk genes’ where having the gene makes the likelihood higher but not guaranteed. Having a parent with Alzheimer’s disease is a risk factor, having more than one relative with Alzheimer’s disease is a high-risk factor.

Clinical Trials are the forefront of research that’s happening with Alzheimer’s today. One study in particular is garnering attention now for changing the period in which they study Alzheimer’s: before the symptoms show up. Scientists are now attempting to treat people who have a high risk to develop Alzheimer’s but are treating them before they display any symptoms of cognitive function loss or memory loss. Through prior studies, it’s now known that Alzheimer’s is often there, in a person’s brain, for ten to twenty years before symptoms show. Their hope is that targeting excess amyloid buildup in a brain before the damage is done to the nerves might delay the onset of Alzheimer’s disease, reduce the damage it causes, or stave off the disease altogether.

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Studying Alzheimer’s in the past and failing to provide any effective treatment in the clinical trials is what led to the change in focus being preventative measures. For some, that’s as simple of a change as taking steps towards heart health with diet and exercise, but for those who have risk or deterministic genes for Alzheimer’s, the outcome of these clinical trials will directly affect their lives.

The course and goal of most prominent clinical trials now is to try drugs that failed the affectability standards for Alzheimer’s patients in all stages of the disease, to instead administer to those who have a genetic predisposition to develop Alzheimer’s disease later in life.

Previous trials preceded the ability to test definitively for Alzheimer’s disease before an autopsy, which meant the sample population had the potential to be people with varying kinds of dementia and not specifically Alzheimer’s disease. Now, PET scans can show researchers which people with dementia have Alzheimer’s disease specifically, so the hope is that the drugs in question weren’t given a fair shot to succeed.

Other researchers now believe that these same drugs that weren’t effective in eliminating or slowing down the progression of Alzheimer’s disease didn’t work because the disease had progressed to far by the time symptoms were showing. These researchers are hoping that since these drugs are proven to break down amyloid or prevent future amyloid from developing, that if they treat a person’s brain before the nerve damage from the amyloid takes place, they can prevent it altogether.

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One of the most interesting fields of study on the forefront of Alzheimer’s disease clinical trials is the one that studies the brains of people from Nordic countries who have a genetic abnormality that hugely decreases their likelihood of developing dementia during aging. The genetic mutation causes an inhibition in the enzyme beta-secretase from producing amyloid protiens. There are drugs that mimic the mutation to inhibit beta-secretase and therefore limit or reduce the amount of amylase and by association, tangles and plaques. The hope is that it’ll reduce the likelihood of people developing the disease by removing the cause.

Alzheimer’s disease is often an intimidating diagnosis since no known cure has been established and it’s prevalence is so high in our society; however, the horizon of research through clinical trials is bright. Progress has been and has continued to be made.

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