How YOU can help stop Alzheimer’s Disease

How YOU can help stop Alzheimer’s Disease


Pretty much everybody knows somebody with
Alzheimer’s Disease. A grandparent, an uncle, a friend’s mom. The disease is distressingly common. And as the Baby Boomer population continues
to age, the number of patients with Alzheimer’s Disease is only going to continue to go up. It exceeds cancer, it exceeds heart disease
with regard to cost to society. With 77 million baby boomers and 10 thousand
people turning 65 every day, the statistics looming ahead for the nation are mind-boggling. Alzheimer’s affects almost five and a half
million Americans and that number expected to triple by the year 2050 to as many as 16
million. There’s 35 million people in the world living
with dementia. And that could double in the next generation,
so we’re talking about a big, big problem. The cost of forgetting is looming as a national
crisis. But if this devastating disease is so common, why haven’t scientists come up with effective treatments? Well, we’ve learned a lot about Alzheimer’s
Disease, but it’s still…complicated. We need to find some sort of sign in the brain
that says, “Hey, this person will likely develop Alzheimer’s”. But at this point, we haven’t identified
a reliable marker that shows up long before any behavioral changes. Nor have we found any treatments that are
effective at preventing them. So what’s the solution? More early clinical research. With more research and clinical trials, we’ll
be able to identify early markers, better understand disease progression, and develop effective treatments. Alzheimer’s Disease, or AD, isn’t just
an effect of aging. It’s a neurodegenerative disorder caused
by biological changes in the brain that ultimately cause the dysfunction and death of neurons. Over time, this leads to memory loss, cognitive
dysfunction, and, ultimately, death. As we talked about in our last video, we do know
something about the biology of AD. Check out that video here if you missed it. But even though we know biomarkers like amyloid
beta plaques and tau tangles are associated with Alzheimer’s Disease, we’re still
not totally sure how, exactly, they lead to the problems seen in the disorder. Like, how does the amyloid beta protein get
misfolded, and why? Why do healthy aging brains also have some amyloid beta plaques that don’t seem to cause any problems? Are the tau tangles part of what causes the
disease, or are they trying to protect the brain, but doing damage instead? It’s hard to answer these questions because,
in part, it’s hard to study Alzheimer’s Disease. In many cases, we use animals like mice and
rats to understand how diseases work. But with AD, animal models don’t cut it. Animals don’t really get dementia the way
we understand it. And they certainly don’t get the same amyloid
beta plaques and tau tangles that we see in Alzheimer’s Disease in humans. In order to model the disease in mice, we
have to introduce genetic mutations that lead to the biomarkers we associate with the disease. But in humans, ordinary AD is almost never
caused by single genetic mutations. These days, most researchers think that Alzheimer’s
Disease is caused by an interaction of environmental and genetic risk factors, and that potential
underlying triggers could include inflammation, infections, and exposure to environmental
toxins. But we’re not exactly sure how those things
combine to cause the disease. So really, we need new research approaches,
including new methods to study it in humans, to fully understand Alzheimer’s Disease. And we especially need to be able to study
people at the very beginning, when the condition first starts to appear. The problem is that we still don’t know very
much about the earliest stages of the disease, and especially how to recognize it before
it has progressed into full-blown dementia. That’s why there’s a push to develop new
ways to study the underlying biology of the condition using human stem cells, animal models
and, most importantly, human research trials. We’ve seen some promising links come out
of this kind of research. For example, scientists have identified new
warning signs of AD, like the genetic variation APOE4, which seems to be a significant risk
factor for developing the condition. Now people who have that particular genetic
variation can let their doctors know that they have an increased risk of developing
Alzheimer’s, and can take preventative measures. The current most effective way to prevent
dementia is by making healthy lifestyle changes. This includes eating a diet high in leafy
green vegetables, whole grains, and lean proteins and low in saturated fats and refined sugar. And getting regular, frequent aerobic exercise. About 30 minutes of moderate exercise five
times a week. Getting plenty of sleep is helpful, too. These habits seem to be helpful in at least
delaying the onset of AD. Likewise, if a patient knows they are at risk, they can stay more aware of any warning signs for the disease. New imaging technologies have allowed researchers
to look directly into patients’ brains to see whether or not they have amyloid beta
plaques or tau tangles, which can help with diagnosing the condition earlier. But imaging technologies are expensive and
are pretty much only used in research settings. As I’ve said before, we still need to work
on finding better markers for the early stages of the disease. Getting larger groups of patients involved
in research trials will allow doctors to compare patient data, find new risk factors, explore
potential biomarkers, and develop improved treatments. Dementia is not just a normal part of aging,
but it’s no surprise that people think it is because we don’t understand aging very
well to begin with. That’s why it’s important for people to
talk to their doctors early and often about their brain health and their risk of dementia. If you talk to your doctor, they can screen
for potential risk factors and early symptoms, and intervene if needed. As people start to get older, they can also
investigate whether or not they might be eligible for longitudinal research studies on Alzheimer’s
Disease and possibly get involved in clinical trials. And that’s really important because remember
that once the damage has happened, there’s no going back. The earlier a patient gets involved in trials,
the more time that gives doctors and scientists to understand how the disease progresses. We also need more early clinical trials to
discover better treatments. Even when doctors can intervene early, there
aren’t a ton of drug options out there for slowing the progression of AD. And most of them don’t work very well in
patients who have progressed further in the disease. New drugs are being developed, but it takes
a long time to get any new medication from the early drug development stages to being
an FDA-approved treatment. And in a disease like Alzheimer’s, which
progresses relatively rapidly, that can make all the difference. So getting more people into early clinical
trials is important for testing new treatments and gathering enough data to determine if
promising therapies are working. Now, it’s important to note here that there
can be some pretty serious barriers that prevent patients from getting involved in clinical
trials or even getting care for early-stage dementia. The first is simply the fear or stigma about
developing AD. It is a scary condition, but knowledge will
be your best defense. Getting involved early means that patients
may help themselves and will definitely help others. Another big barrier is that physicians have
limited time, resources, and motivation to screen patients and refer them to trials. If you encounter this, push your physician
for a referral or seek out a doctor who has the resources to help you. Likewise, living in a rural or low-income
area can make it difficult to access health insurance and health care, or may mean there
are fewer medical centers, making it nearly impossible for aging patients to access early
intervention treatments. And when people live alone, it can be hard
for them to notice on their own when symptoms start to show up. So maintaining a strong social network is
important for helping recognize the early stages of AD. Check-in on your elderly family members and
neighbors. They might appreciate it. Another barrier to clinical trials is…people
just don’t know about them. Building awareness is something we can all do by talking about these kinds of trials with others. And a lot of other folks, like Bill Gates,
are trying to increase awareness and accessibility of early clinical trial opportunities among
doctors and the public so that more patients can get enrolled. Some resources for that include the National Institute on Aging’s Clinical Trials finder. And if you’re in the UK, the Join Dementia
Research program. Check out the links in the description for
more info. While we have not discovered any very effective
treatments yet, we do know for certain that the first time a case of Alzheimer’s Disease
is successfully averted, it will be thanks to a clinical trial. So I encourage you to learn more about these
early intervention clinical trials and think about whether or not you or a loved one can get involved in helping us find a way to prevent this terrible disorder. Talk to your aging family members about the
warning signs of dementia, and make sure they know the basics of Alzheimer’s Disease. You could even share both of our videos with
them, even if they’re completely healthy. Thank you again to the office of Bill Gates
for their help and support making this video. Bill is on a mission to generate more awareness
about Alzheimer’s Disease research and helping aging adults get involved in clinical
trials. To learn more about clinical trials and enrollment
near you, check out the links below. As someone who lost a family member to dementia,
I’m happy to help raise awareness about clinical research to find treatments so that others don’t have to experience that same kind of loss. Thanks for watching this episode of Neuro
Transmissions. I’m Alie Astrocyte, and until our next transmission,
over and out!

10 thoughts on “How YOU can help stop Alzheimer’s Disease

  1. One of the strongest early biological predictors is Insulin Resistance, is that not why Neuroscientists often call Alzheimer's type 3 diabetes?

  2. I am ready to be a clinical #trial in your location. I believe I am getting it too. My #Father currently faces #alzhiemers in India and he is 75 now and there are some #centres in India where they just help in #socializing or collecting the people and spreading the knowledge facing Alzheimer's but it should be AT A MUCH GREATER LEVEL IN EVERY CITY and I believe I and my father suffered a lot when we did see my #grandfather having the same as well and that I could see as that he forgot his own kids when seeing them etc and had to be reminded who is standing in front of him etc but #how do I get the #cure for the same for my father #before it gets too bad and I am #scared #daily cause I do not know how to prevent it for myself and I do know this though that my #memory is not great and I have #forgotten my #childhood completely .. I hardly remember my days except very few things of my childhood and in today's time I #forget where I have kept what etc after few days or sometimes immediately.. my father ofcourse forgets what he just heard or just spoke and repeats the same question again ! HOW DO I #CONTRIBUTE #MYSELF INTO THIS FIELD ! I am ready to #donate #myself for tests and I want to prevent my Dad from going worse!

  3. Thanks for sn intetesting clip. Did you read the article in the New Scientist around 2017 about Rem sleep, NRem 1, Nrem 2, Nrem 3 and Nrem 4 and the sleep types influencing the brains 'cleaning' systems? There had been some human trials and the test had the ability to bring people up from deep delta wave sleep to REM sleep (using sound) and how that made a distinct difference to memory recall and storage. I think it was called "Does Insomnia cause Alzheimer?" I found it an interesting article and was hoping to see some development in that research. The article made me think about the possibility of being able to stimulate NREM type 4 sleep (possibly with sound) to aid better brain cleaning stimulation while sleeping.

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