You might think that dementia is something
that happens when you get old. The brain just...starts to break down, right? And yet, 60 to 80% of all dementia cases are actually Alzheimer’s Disease. A devastating condition that can seemingly erase the minds and memories of your loved ones right before your eyes. Alzheimer’s Disease is not just a normal
part of aging. So let’s talk about what we know and how the future of Alzheimer’s research looks bright thanks to early intervention clinical
trials. Hey Brainiacs! It’s me, Alie Astrocyte, back at it again. Alzheimer’s Disease, or AD, is what’s
known as a neurodegenerative disorder, which is pretty much exactly what it sounds like. Any condition that causes the loss of function or death of neurons. Because we don’t grow many new neurons as
adults, neurodegenerative conditions are usually very serious, and generally fatal. Alzheimer’s Disease is no exception. The average life expectancy after an AD diagnosis is only about 4-8 years. Part of the reason some people believe that Alzheimer’s Disease is a “normal” part of aging is probably because it’s strongly correlated with getting older. The condition affects 1 in 10 people over the age of 65. But it can sometimes strike at a younger age and has been diagnosed in some people in their 20’s. While all Alzheimer’s Disease patients end
up with what we call dementia, not all kinds of dementia are a result of Alzheimer’s Disease. Dementia just refers to the loss of memory and cognitive abilities that accompany the neurodegeneration. This condition presents a pretty big challenge
to scientists and doctors today. As you’re probably aware from the amount
of attention it receives in the media, AD cases are on the rise in the U.S. Mostly as a result of the aging Baby Boomer population. And it frequently isn’t detected until patients
are in advanced stages of the disease, because their cognitive issues are often chalked up
to aging, and because we don’t have good tools to detect the disease before people start to change their behavior. That means that lots of patients don’t know they’re sick until their brains have already been badly damaged. But, it’s not all doom and gloom. Scientists believe that earlier intervention
can help slow dementia’s progress. And the earlier you intervene in the progression of
the disease, the better the outcome for patients. Thousands of scientists and doctors are hard at work developing new ways to identify Alzheimer’s Disease earlier and earlier, and to create treatments to help protect our brains. So what causes Alzheimer’s Disease? The biology is still not entirely clear, but
what we do know is that there are two key biomarkers that appear to be tied to the condition. First, we have amyloid beta plaques. Amyloid beta is actually a broken off piece
of a protein called amyloid precursor protein, or APP. The role of APP in the brain also isn’t well
understood, but there’s pretty good evidence that it’s important for normal brain development and synapse function. In Alzheimer’s Disease, amyloid beta gets
misfolded, so the protein is misshapen, and can’t be processed correctly by the brain. The amyloid beta then builds up into amyloid
plaques in the space around neurons. We’re not sure exactly why, but something about that protein build up is toxic to the brain. Amyloid beta plaques lead to apoptosis, or programmed cell death, changes in glucose metabolism, and increased inflammation, which
are all thought to contribute to the progression of the disease. Another kind of marker for Alzheimer’s Disease
are the tau tangles. Tau is a structural protein found inside neurons. Normally tau is a good thing. But in AD, there are changes in how the tau protein is processed, which cause it to form abnormal clumps called tangles. These tangles are thought to damage the structural
integrity of the cells and make it hard for the neurons to support themselves. Together, the amyloid beta plaques and tau tangles appear to play a role in neuronal death and the reduction in the number of synapses, which leads to the symptoms of the disorder. And unfortunately, there is no cure for the
disease. Once those brain cells are gone, they’re gone. The research so far suggests that these biological changes in the brain appear before the cognitive symptoms. These proteins first build up before
they start causing problems. That means that the sooner doctors can detect these biomarkers, the sooner they can start treating patients, and slow down or maybe even prevent the disease. But to do that, doctors and researchers need to access patients earlier in the disease progression to start addressing some of these challenges. We need to figure out why it is that amyloid
beta plaques form in normal aging brains, and why some patients with these plaques go
on to develop AD while others may not. We also need to better understand what role
tau tangles have in the condition. There’s some evidence that they damage neuronal
structures, but some scientists think that the tau tangles might actually be a protective response. It’s not until cells start to die that tau tangles start to appear. So there’s a possibility that, like a sort of autoimmune disorder, the tau tangles are trying to help, but end up hurting instead. We can do some Alzheimer’s research using
animal and tissue models, but Alzheimer's is a uniquely human disease. If we really want to understand
what’s going on in the brain, there need to be more human research trials, and more enrollment in the early clinical trials to test new interventions and treatments before
the damage has been done. These efforts will help scientists identify
earlier biomarkers and symptoms that signal the onset of the condition, so doctors can
start providing intervention treatments sooner. And, more importantly, allow doctors to test
new treatments. And because we can’t reverse dementia once the neurons have died, it’s really critical that patients get enrolled in clinical trials when they’re still early in the disease progression, to help scientists understand what can be done to actually slow down the condition. So if you’re approaching the age of 65,
or have already passed that benchmark, talk to your doctor about Alzheimer’s disease,
cognitive screening, and how you can get involved in the research. Even if you’re perfectly healthy, it’s
important for folks like you to get involved, because we need to understand normal aging in order to understand what’s going wrong in AD. For younger folks, I encourage you to talk
to your aging family members about the risk factors for dementia. Encourage them to talk to their doctor about
cognitive screening, which can help identify participants for clinical trials. Especially
if you have a family history of Alzheimer’s, and especially if there’s a history of early
onset AD. If you can, help aging family members look
into resources for finding and participating in research trials in their area. Check out some of the links in the description
to start your search, including the National Institute on Aging’s Clinical Trials finder. We’d like to thank the office of Bill Gates for their
help and support making this video. Bill is dedicated to helping raise awareness about the challenges facing Alzheimer’s Disease research and helping more aging adults get involved in research studies. If you're interested in learning more about clinical trials and enrollment near you, check out the links below for more information and resources. Thanks for watching this episode of Neuro
Transmissions! If you haven’t already, subscribe and hit that bell button to see all our new brainy videos when they come out. And if you've had your own experience with Alzheimer’s feel free to leave your story in the comments below. It’s a challenging disease, but together
we can find effective treatments. I’m Alie Astrocyte, and until our next transmission,
over and out!
