BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Alzheimer’s (Page 1 of 2)

Can Alzheimer’s Disease be Transmitted?

https://www.flickr.com/photos/institut-douglas/2677257668

We have long associated Alzheimer’s disease as a condition that could come with aging, but have you ever thought that the disease could also be transmitted? 

 

In most cases, Alzheimer’s disease affects an older population group, as around 1 in every 9 people who are aged 65 or older in the US have Alzheimer’s. However, in January 2024, researchers have reported in the Nature journal that five people who received contaminated injections of a growth hormone in their early childhood years came to develop Alzherimer’s disease unusually early – between ages 38 and 55. This points to the potential that the contamination of the growth hormones to be a cause of the unusually early development of Alzheimer’s disease in the 5 people reported. 

 

These 5 people received hormone injections that are used to treat various growth disorders. The hormones are extracted from pituitary glands of cadavers (a practice no longer used), as the pituitary gland is the location in the body that produces growth hormones that signals the body for growth. However, sometimes these extractions are contaminated with infectious, misshapen proteins, which could cause serious problems in human cells such as preventing the cells from doing its regular jobs to forming clumps in cells. 

 

One of these infectious proteins that came along with the extracted growth hormones from pituitary glands of cadavers is the amyloid-beta protein, which research shows is a hallmark of Alzheimer’s disease as it accumulates in the brain. In class, we learned about the importance of growth hormone proteins in stimulating cell growth. When cells receive growth hormone signals, they are stimulated to keep dividing and growing, and conversely when they don’t, they will stop the cell reproduction cycle. However, for patients who were contaminated with the A-beta growth hormone protein, some harmful cells in their body would be instructed to keep on growing, dividing, and continuing their reproduction cycle, which could be a possible cause of Alzheimer’s disease. 

 

After learning about how it’s possible that Alzheimer’s disease could be developed through medical contaminations, what are some improvements you think should be made in medical settings that could prevent future situations similar to this?



The Blood Brain Barrier Can’t Block This!

University of Wisconsin-Madison Professor, Shaoqin “Sarah” Gong is ready to take on finding cures for brain disease such as Alzheimer’s and Parkinson’s disease. Gong and her colleagues strive to enable a “noninvasive, safe and efficient delivery of CRISPR genome editors” that can be used as forms of therapy for these diseases. According to MedlinePlus, there are many forms of brain disease, some caused by tumor, injury, genetics; however, Gong’s research focuses on degenerative nerve diseases. Degenerative nerve diseases can affect balance, movement, talking, breathing and heart function. The reason cures for degenerative nerve disease are difficult to create is because of the blood brain barrier. According to the American Society for MicroBiology, the blood brain barrier is a feature of the brain and central nervous system blocking the entrance of “microorganisms, such as bacteria, fungi, viruses or parasites, that may be circulating in the bloodstream”. Unfortunately, the barrier block is a very selective site that won’t let vaccines and therapies through. Fortunately, Gong’s nano-capsules with CRISPR’s genome editors point toward brain disease therapy and a cure.

 

Alzheimer's disease brain comparison

Gong’s study proposes dissolvable nano sized capsules that can carry CRISPR genome editing tools into organs. According to CRISPR Therapeutics, CRISPR technology meaning Clustered Regularly Interspaced Short Palindromic Repeats is an “efficient and versatile gene-editing technology we can harness to modify, delete or correct precise regions of our DNA”. CRISPR edits genes by “precisely cutting DNA and then letting natural DNA repair processes take over.” CRISPR targets mutated segments of DNA that can produce abnormal protein causing diseases such as degenerative nerve disease.  CRISPR works with the help of a guide RNA and Cas9. Together the complex can recognize and bind to a site next to a specific target sequence of DNA that would lead to the production of an abnormal protein. CAS9 can cut the DNA and remove a segment. As a result natural DNA pathways occur and RNA polymerase will return to rebuild and correct the mutated segment. 

via GIPHY

Consequently with the addition of glucose and amino acids the nano-capsules containing CRISPR Technology can pass through the blood brain barrier to conduct gene editing to target the gene for the amyloid precursor protein that is associated with Alzheimer’s. The topic of gene editing coincides with the Gene Expression portion of the AP Biology curriculum. In the topic of gene expressions 2 processes are emphasized: transcription (the process of making an RNA copy of DNA) and translation ( the process of making proteins using genetic information from RNA). In the CRISPR technology the editing of genes closely relates to the process of transcription. Transcription mistakes can be made which can lead to mutations, these mutations can potentially cause nonsense, missense or deletions of nucleotides ultimately producing wrong codons that would code for incorrect/abnormal proteins. However, the CRISPR technology would be able to correct these mutations in the DNA, replacing the incorrect nucleotides to correct ones and preventing the production of abnormal proteins. Fortunately, Gong’s unique nano-capsules have successfully been tested on mice, giving scientists hope that treatments and therapy for these brain diseases are coming soon and can help many.

Can this Protein Cause Alzheimer’s?

What causes Alzheimer’s? Initially, one might think that it is a result of age-related changes in the brain or environmental and lifestyle changes. One may also think that it is caused by a genetic predisposition to the disease. Personally, I thought Alzheimer’s was a result of poor health as one got older. Although these all may be true, a new study has found that Alzheimer’s Disease can be caused by a certain protein, or rather, a protein mutation. These new findings provide scientists with a way to detect and treat the disease in the long run.  Using multiple methods to analyze mitochondrial DNA, researchers found a mitochondria microprotein that is associated with Alzheimer’s Disease. This protein, known as SHMOOSE is seen to have a role in the neurodegeneration of people, thus giving them an increased chance of Alzheimer’s Disease. Furthermore, the researchers found that the microprotein is found in over a quarter of Europeans. The researchers of The Cohen Laboratory at the University of Southern California published their findings in the journal of Molecular Psychiatry. The journal states that the microprotein, SHMOOSE was discovered through the use of neuroimaging, mass spectrometry, and transcriptomic. All of these are methods of looking into the mitochondrial DNA and locating the mutated protein. According to the study, a mutation of the SHMOOSE microprotein has a connection to a higher risk for Alzheimer’s Disease. They also discovered that 25% of individuals with European ancestry have the mutated version of the protein. Dr. Pinchas Cohen says that the SHMOOSE mutation is a result of a single nucleotide polymorphism or SNP. An SNP is essentially a change or alteration within a single nucleotide, in this case, the change resulted in the mutated SHMOOSE protein. Additionally, he states that the variant can guide ways to identify who is affected while also forming new medical treatments and preventative measures. In class, we learned about how proteins are created and coded for, and we also learned about how protein structure directly affects their function. Both of these concepts are directly seen in this study. Firstly, DNA is what codes for proteins, if the DNA or even the nucleotide is incorrect or altered, the protein would in turn also be incorrect or altered. This is seen directly through the SNP, the single change in the nucleotide entirely changed the protein creating the SHMOOSE protein. Next, the structure of the protein, the sequence of the amino acids, or just the overall composition of the protein entirely plays a role in the function and actions of the protein. For example, if the structure of a protein is compromised, so is the function. This is also directly seen in the study because the structure of the SHMOOSE protein was altered due to the SNP, its function was also altered. The altered function is that it would put people at a higher risk for Alzheimer’s Disease. Another article speaks on the silver lining of the SHMOOSE protein. Because the protein is the approximate size of an insulin peptide, it could easily be administered into the human body for a positive effect. This means that the mutated protein could be used for treating Alzheimer’s Disease and increasing its therapeutic value. This idea is just one of many that venture into the field of precision-based medicine. In the case of Alzheimer’s the mutated SHMOOSE would be focused upon as a target area rather than the disease as a whole. I think that the use of SHMOOSE in a medical or therapeutic way would be risky at first in that it would likely be difficult for scientists to specifically target the way to treat it. What may be a safer option for those with the mutation could be to continue with tried and tested Alzheimer’s Disease treatments rather than immediately opting for something new. The new precision-based medicine method should undergo severe trials, examinations, and successes before it is widely implemented.

 

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Can Your Eyes Save Your Brain?

Are Retinal Tests Able to Identify Early-Onset Alzheimer’s?

According to The Alzheimer’s Association, In 2021, 6.2 million Americans were living with Alzheimer’s Disease. 1 in every 9 people (11.3%) above the age of 65 has Alzheimer’s Disease, and these percentages only increase with age, leaving 35 percent of people above the age of 85 with Alzheimer’s or Dementia. For those who do not know, Dementia is a general term for the loss of memory and other thinking abilities, severe enough to interfere with daily life. Alzheimer’s is the most common type of Dementia, and it affects not just memory but behavior. Mainly recognized in adults above the age of 60, our current form of diagnosing Alzheimer’s is waiting until people become overly forgetful or begin to act out of character. Although early detection is occasionally possible through brain scans, this method is expensive and unsuitable for most. 

My uncle Steven was only 51 when he was diagnosed with Alzheimer’s. Although caught decently early, his changes in behavior and short-term memory loss were apparent. Often asking a question only minutes after he had previously been told the answer, my family was devastated. Before being diagnosed, my uncle was the CFO of a Fortune 500 company and was always seen as a mentally and physically strong man. Having no choice but to retire young and focus on his health was a hard truth for all of us to accept. 

Alzheimer's Disease

Sad and confused about how this had happened, I did extensive research on the causes of Alzheimer’s. Although there are multiple possible causes and factors that play into the development of Alzheimer’s disease, one way is through inheritance. Early-onset Alzheimer’s diseases, like my uncle’s, can be inherited genetically. Humans typically have 46 chromosomes in each cell of their body. Each of these chromosomes contains anywhere between 20,000 and 250,000 genes. Usually having two copies of each chromosome, one copy comes from the mother’s egg and the other from the father’s sperm. Each egg and the sperm are haploid, meaning they contain 23 chromosomes. When the sperm fertilizes the egg, two copies of each chromosome and gene are present. Although some genes are required from both parents to be passed onto their offspring, Alzheimer’s is inherited in an autosomal dominant pattern. This is one of the many ways that disorders can be passed down through families, and it means that only one parent needs to have the abnormal gene for you to get the disease. Thus people who inherit one copy of the APOE e4 allele have a significant chance of developing Alzheimer’s. However, those who inherit two copies of their allele are at even greater risk. It is important to note that not all people with the disease have the e4 allele, and not all people with the allele develop Alzheimer’s. Because in most cases, an infected person inherits the gene from an infected parent, it is not likely that my uncle developed Alzheimer’s genetically as no one else in my family tree ever had the disease.

Autosomal dominant inheritance

Moving forward with my research, I looked into possible treatments; unfortunately, most drugs are still in trial or only applicable to individuals diagnosed before any level of severe memory loss occurs. While this is a sign of good progress, I can’t help but feel there must be some better solution to diagnose Alzheimer’s before it becomes too late. Thankfully, Dr. Ashleigh Barrett-Young and her team agreed.

Working at Otago’s Dunedin Multidisciplinary Health and Development Research Unit, Barrett-Young and her team of researchers have investigated the retina’s potential to indicate Alzheimer’s earlier in life. As stated by Barrett-Young, “In the near future, it’s hoped that artificial intelligence will be able to take an image of a person’s retina and determine whether that person is at risk for Alzheimer’s long before they begin showing symptoms, and when there is a possibility of treatment to mitigate the symptoms.” The Dunedin study analyzed the retinal nerve fiber layer (RNFL) and Ganglion cell layer (GCL) of 865 people at the age of 45. Dr. Barret-Young and her team reported that thicker RNFL and GCL were associated with better cognitive performance, while a thinner RNFL was linked to a more significant decline in processing speed. Adding to their report, “These findings suggest that RNFL could be an indicator of overall brain health. This highlights the potential for optical scans to aid in the diagnosis of cognitive decline.” Since treatment for Alzheimer’s is yet to be discovered, the ability to identify the disease in preclinical stages could allow the possibility of aid before it’s too late. Although further studies are required to determine if retinal scans can predict precisely Alzheimer’s, or just the expected cognitive decline of the brain, researchers have hope. 

So, while this solution sadly offers no benefit to my uncle, I feel hopeful that this new diagnosis technique will be beneficial for the millions of people who would have had family members or friends combating Alzheimer’s disease but caught it early enough to intervene and do something about it. 

Our Circadian Rhythm Could Affect Alzheimer’s Disease

The National Institute of General Medical Sciences defines the circadian rhythm by our behavioral changes that follow a twenty-four-hour cycle heavily influenced by light and dark periods (NHS.GOV). Whether these changes are physical, mental, or behavioral, our circadian rhythm is critical for our survival as a species. The most important way of maintaining an efficient circadian rhythm pattern is by having a consistent sleep schedule, as explained by the scientists at Rensselaer Polytechnic Institute. Your body can adequately enter Delta (slow-wave) sleep by having a consistent sleep schedule. This sleep cycle is the most crucial out of them all, for it is when your body achieves maximum restoration and when your mind can sufficiently rest.Circadian rhythm in a human

But what else does our body’s circadian rhythm do for us? Well, scientists at the Rensselaer Polytechnic Institute have uncovered a possible correlation between Alzheimer’s disease symptoms and our circadian rhythm. Essentially, they have discovered that “the circadian system is composed of a core set of clock proteins that anticipate the day/night cycle by causing daily oscillations in the levels of enzymes and hormones, ultimately affecting physiological parameters such as the immune response” (RPI). Furthermore, diseases such as Alzheimer’s and diabetes become far more prevalent when the circadian rhythm is interrupted.

Microscopic signs of Alzheimer'sSo then, what exactly happens on the molecular level? How does disruption of the circadian rhythm influence diseases such as Alzheimer’s? As we’ve learned through the Immune System unit, macrophages engulf unwanted foreign invaders, which is one of the most critical aspects of our immune system. In the case of Alzheimer’s, one telltale is the formation of extracellular clumps of AB42, the 42 amino acid form of amyloid-β, around the brain which macrophages would typically engulf through phagocytosis (NIH.GOV). Further, “the researchers noticed oscillations in enzymes that help to make two proteins on the macrophage cell surface — heparan sulfate proteoglycan and chondroitin sulfate proteoglycan- both of which are known to play a role in regulating clearance of AB42” (RPI). As explained in the previous paragraph, if a disruption of the circadian rhythm affects our body’s immune response, this indeed entails that a disease like Alzheimer’s would only worsen over time, assuming that no regulation of the circadian rhythm would take place.

The findings seem promising, especially for a disease like Alzheimer’s which has no known cure yet. Only medicines that reduce symptoms are currently in circulation which just isn’t sufficient especially since Alzheimer’s is a prominent issue within older citizens. If scientists are able to further utilize this knowledge to help prevent Alzheimer’s from reaching high severity, then hopefully the lives of many will be improved and Alzheimer’s can be a disease of the past!

How a Rogue Protein can cause Alzheimer’s Disease

In a study done by NYU Langone Healthy and the School of Medicine, researchers learned more about the types of proteins that cause the tangles in the brain that cause Alzheimer’s. Alzheimer’s disease is a type of dementia that affects the “memory, thinking, and behavior” of the over 5 million Americans who have it, according the the Alzheimer’s Association. The researchers tested tissue sample of 12 subjects with the disease looking for tau knots to “[examine] the bundles to identify the many proteins tangled within”.

File:Histopathology of neurofibrillary tangles in Alzheimer's disease.jpg

Shown is the tangles that are found in and contribute to Alzheimer’s disease 

You might be wondering, what is a tau knot? A tau is a protein that exists mostly in nerves that has the objective of stabilizing microtubules. When this protein is defective, it can become tangled with other molecules which leaders to Alzheimer’s disease.

Although neuroscientists already knew that tau tangles can cause neurodegenerative diseases like Alzheimer’s or dementia, they did not know many of the proteins that cause these dangerous knots. After analyzing the brain tissue, the researchers “found 12 proteins that they say have not before been tied to both tau and Alzheimer’s disease.” These knots were made up of 542 different proteins including those involved in the most essential processes of the cell like “energy production”, “the reading of genetic material”, “and cell breakdown and digestion.” These proteins that work to produce ATP and RNA in the processes of cell respiration and gene transcription (which are necessary parts of cell function); these important proteins are involved in the knotting. It is crazy that along with their existence comes the possibility of them destroying all they have created.

Despite the sad nature of this research, this new information comes along with hope for those suffering from this debilitating illness. According to co-lead author Geoffrey Pires, “Now that we have better insight into possible ‘key players’ in neurodegeneration, we may have clearer targets for potential therapies.” As these researchers gain more and more information, they gain a better understanding of Alzheimer’s and in turn, other similar “tau-linked neurodegenerative diseases, such as Pick’s disease.”

I feel Alzheimer’s is an essential disease to learn more about not only because it is incurable and unpreventable, but because 4 members of my own family have suffered from it. As the study’s senior author Thomas Wisniewski said “Alzheimer’s has been studied for over a century, so it is eye opening that we are still uncovering dozens of proteins that we had no idea are associated with the disease.” It is wild to think that something so common and well known, still has so many mysteries to it and that makes it immensely more fascinating and important to learn about.

Eating Shark Meat Increases Your Chance At Developing Alzheimer’s Disease

What toxins lie beneath the grey leathery skin of a shark? 

According to the article written at the University of Miami Rosenstiel School of Marine & Atmospheric Science,  scientists found toxins that are commonly linked to neurodegenerative diseases in the fins and muscles of many different types of sharks. Scientists collected samples of ten different sharks that are commonly found in the Atlantic and Pacific Ocean. The samples came back and tested positive for two toxins: mercury and beta-N-methylamino-L-alanine(BMAA). Many studies have linked mercury and BMAA to diseases like Alzheimer’s and amyotrophic lateral sclerosis(ALS). Shark meat delicacies are common in many Asian countries with dishes including shark fin soup.

Effects of Mercury on humans

Mercury has numerous health effects on humans and can be detrimental to one’s neurological system. Not only that, mercury also affects digestive and immune systems and can damage lungs, kidneys, skin and eyes. Mercury poisoning can also cause slow reflexes, damaged motor skills and intelligence disorders. In many instances, mercury poisoning can increase your chance at developing Alzheimer’s disease. Researchers found that the toxin mercury tends to accumulate in the shark’s tissue throughout their lives.

Effects of beta-N-Methylamino-L-alanine (BMAA) on humans 

The neurotoxin beta-N-Methylamino-L-alanine is an amino acid produced by certain organisms that have been linked to ALS, amyotrophic lateral sclerosis. BMAA was also linked to being a cause of Parkinson’s disease. Researchers found BMAA in shark fins and cartilage both of which are used in food and medicine, respectively. The image shown below is of alanine, one of the amino acids. There is an NCC structure shown in the middle, a carboxyl group on the left hand side, an amine group on the right hand side and the CH3 represents the R group. Since BMAA is a non-protein amino acid, when inserted with other amino acids it releases toxic chemicals. The picture below represents an alanine amino acid, however, BMAA has a slightly different structure. The R group of BMAA is NH along with H3C and the amine group is NH2 which contributes to its toxicity.

Why you shouldn’t eat shark meat? 

If the reasons above have not convinced you not to eat shark meat, many species of sharks are facing extinction due to the high demand for shark parts. Though each of these toxins have their own set of dangers, mercury and BMAA together can have an entirely different and more dangerous effect on humans that researchers have not yet explored. To be safe one should refrain from consuming shark products if not for your own health but to save the sharks.

Don’t be afraid of sharks we need them! 

Sharks play a very important role in the ecosystem. Sharks are the apex predators in marine life are most likely at the top of the food chain. Ultimately, they keep the rest of the ocean healthy and in order. Without them many dangerous organisms would be present and could harm marine life. Sharks keep balance within the ecosystem and ensures diversity among ocean species. If you suffer from viruses like cystic fibrosis, researchers are close to finding anticoagulants within shark tissue that could possibly cure certain diseases. Sharks are also very important in the carbon cycle. When they die naturally, their bodies are full of carbon which is then consumed by scavengers and carbon is recycled into the ecosystem. Sharks do way more for us than we think!

Does This Protein Trigger Alzheimer’s Disease?

Research done by scientists at the Instituto de Neurociencias de Alicante, in Spain has revealed that the way people with Alzheimer’s process a key protein may lead to the creation of new tests and maybe even treatments. Alzheimer’s disease is a common form of dementia, where memory and thinking skills are progressively lost.

People with Alzheimers have a build up of insoluble plaques made of beta-amyloid and tau, both are proteins. Beta-amyloid is a part of a much larger protein called amyloid precursor protein, which is otherwise known as APP. APP is broken down by enzymes into either a beta-amyloid fragment, which is harmful, and causes Alzheimers, or another harmless fragment.

The process of the beta-amyloids forming insoluble plaques.

Glycosylation is the process of adding sugars to proteins, to form a glycoprotein, during production and the location of these sugar molecules is important in determining the ultimate destination of the protein in the cell. The glycosylation of the amyloid is altered in the brain of an Alzheimer’s patient, research suggests. Therefore, the protein is being processed in such a way where more beta-amyloid is being produced. This mutation no matter how small, can play a huge role in how the protein functions. Proteins have a unique shape determined by the interactions of their side chains. The shape the protein forms usually has to match with another molecule or structure. If the structure is mutated in any way, the protein may not remain the same shape and therefore not match the shape of another molecule or structure. This causes a change in the function. Therefore in this case with amyloid, how the protein is glycosylated will determine where it ends up in the cell membrane, due to shape and this will determine if an enzyme will break it down or not. 

The research found a difference between Alzheimer and non-alzheimer patients in terms of how APP is glycosylated. The patterns of APP glycosylation were evidently different. The patterns of proteins are so crucial to their function and structure. So, researchers were able to perform a chemical analysis and found that these different patterns may be a result of different processing of the protein. By processing APP differently, it may trigger Alzheimers. The protein structure is changed and the protein will not act the same. Therefore, with this knowledge, by looking for APP that has an altered way of being glycosylated, it may be easier to detect Alzheimers and inspire treatments in the future. This research is so exciting and important because one day it can help with Alzheimer’s treatments. Not only will it be a great detection test, but the by preventing the creation of beta-amyloid Alzheimers may be preventable in the future or easier to spot. Do you think this sounds like a promising next step to Alzheimer’s detection and treatment?

Can your diet’s effect on gut bacteria play a role in reducing Alzheimer’s risk?

Could following a certain type of diet affect the gut microbiome in ways that decrease the risk of Alzheimer’s disease? According to researchers at Wake Forest School of Medicine, that is a possibility.

In a small study, researchers were able to identify several distinct gut microbiome signatures in study participants with mild cognitive impairment (MCI), but not in the other participants with normal cognition. Researchers found that these bacterial signatures correlated with higher levels of markers of Alzheimer’s disease in the cerebrospinal fluid of the participants with MCI. Additionally, through cross-group dietary intervention, the study also revealed that a modified Mediterranean-ketogenic diet resulted in changes in the gut microbiome and its metabolites that correlated with reduced levels of Alzheimer’s markers in the members of both study groups.

“The relationship of the gut microbiome and diet to neurodegenerative diseases has recently received considerable attention, and this study suggests that Alzheimer’s disease is associated with specific changes in gut bacteria and that a type of ketogenic Mediterranean diet can affect the microbiome in ways that could impact the development of dementia,” said Hariom Yadav, Ph.D., assistant professor of molecular medicine at Wake Forest School of Medicine.

The randomized, double-blind, single-site study involved 17 older adults, 11 diagnosed with MCI and six with normal cognition. These participants were randomly assigned to follow either the low-carbohydrate modified Mediterranean-ketogenic diet or a low-fat, higher carbohydrate diet for six weeks then, after a six week “washout” period, to switch to the other diet. Gut microbiome, fecal short chain fatty acids, and markers of Alzheimer’s in the cerebrospinal fluid were measured before and after each dieting period.

The limitations of the study included the subject’s group size, which also accountns for the lack of diversity in terms of gender, ethnicity, and age.

“Our findings provide important information that future interventional and clinical studies can be based on,” Yadav said. “Determining the specific role these gut microbiome signatures have in the progression of Alzheimer’s disease could lead to novel nutritional and therapeutic approaches that would be effective against the disease.”

Each human contains trillions of organisms that influence our metabolism, immune function, weight, and even cognitive health. It is so fascinating to examine the role of gut microbiomes in the progression of Alzheimer’s disease. I believe diets can be very controversial, and I find it interesting to see researchers in this study show how the Mediterranean-ketogenic diet may be effective against Alzheimer’s. However, I am so intrigued to see where these findings may take us with approaches that may be effective against Alzheimer’s, whether they be nutritional or therapeutic approaches.

Can you get a disease from being outside?

The Alzheimer’s diseases and several genetic defects have been identified to connect with early onset family genetics. In this study chemists, toxicologists, and biologists have researched the environmental effects connected with health issues. The researchers examined the point that the human race would have all gone extinct if our bodies didn’t have the ability to metabolize, absorb, or excrete trace substances. In 2005, there was a lot of talk about the “exposome” causing many diseases. This research topic is very  interesting because it explains that everything you are exposed to can cause cancer. The fact that our exposome is everything we contact in our lives is concerning. Average light, invisible car exhaust and ambient street noise are all linked to birth defects. And now Alzheimer’s has been statistically linked to the environment.

Although Alzheimer’s is generally linked with age, researchers also believe it is linked to living in cities and poorer neighborhoods. According to new research unveiled at a recent global gathering of Alzheimer’s experts in London, stressful life events, poverty and racial inequities contribute to dementia risk in late life. A Study at the University of Wisconsin looked at levels of socioeconomic disadvantages such as poverty, education, housing, and employment to determine whether there was a stronger link to developing Alzheimer’s than by chance alone. They found that people in poor neighborhoods had worse cognitive performances in all aspects, which is linked to the fact that they had disproportionately higher levels of the Alzheimers disease biomarker in their spinal fluid. This could be considered an example of the effects that their exposome pose on their health. For example, in poorer neighborhoods, they have less access to healthy foods, safe exercisee options and healthy environments. This unhealthy environment leads to increased risk of diabetes,  cancer, and early death.

A Good Night’s Rest is More Important than We Thought: Decreased Slow-Wave Sleep Linked with Alzheimer’s Disease

Whether it be a quick nap or a nighttime full of sleep, I love sleep. However, with a busy schedule and tons of commitments, I find myself prioritizing these events over my own rest. How much do these short-term habits affect your long-term health?

It has been noted that poor sleep is a telltale symptom of Alzheimer’s disease. As the disease progresses, people tend to wake up tired and their sleep becomes less refreshing. But, is unclear how and why restless nights are linked to Alzheimer’s disease. However, researchers at Washington University School of Medicine in St. Louis may have discovered part of the explanation.

Alzheimer’s disease affects approximately 5.7 million Americans, and the brain changes appear slowly and silently. Up to two decades before the characteristic signs of memory loss and confusion appear, amyloid beta protein begins to build up into plaques in the brain. The brain protein tau appear later, then atrophy of the key brain areas next. It is after all of these internal and unnoticeable changes that people start to show unmistakable symptoms of cognitive decline. But, what if there were a way to find the symptoms earlier?

The researchers at Washington University in St. Louis found that older people who have less slow-wave sleep, the deep sleep your body needs to consolidate memories and wake up feeling energized, have higher levels of the brain protein tau. Elevated levels of it has been linked to brain damage and cognitive decline, such as in Alzheimer’s. The relationship between sleep, the tau protein, and Alzheimer’s marks great strides in diagnosing and helping patients with the disease. Brendan Lucey, MD, an assistant professor of neurology and director of the Washington University Sleep Medicine Center believes that “measuring how people sleep may be a noninvasive way to screen for Alzheimer’s disease before or just as people begin to develop problems with memory and thinking.”

Decreased slow-wave sleep and increased production of the tau and amyloid proteins have been linked to Alzheimer’s disease.

The study examined 119 people 60 years of age or older. Researchers monitored the participants’ sleep through a portable EEG monitor that strapped to their foreheads to measure brain waves, as well as a wristwatch-like sensor that tracked body movements. Participants also kept sleep logs, making note of both nighttime sleep and daytime naps. Additionally, researchers measured levels of amyloid beta and tau in the brain and spinal fluid. The results found that decreased slow-wave sleep coincided with higher levels of tau and amyloid. Lucey remarked that “the key is that it wasn’t the total amount of sleep that was linked to tau, it was the slow-wave sleep, which reflects quality of sleep. The people with increased tau pathology were actually sleeping more at night and napping more in the day, but they weren’t getting as good quality sleep.” In fact, daytime napping was significantly associated with high levels of tau.

This newfound information concludes that sleep monitoring may be an easy and affordable way to screen earlier for Alzheimer’s disease. Doctor’s may be able to ask a simple question: “How much do you nap during the day?” to identify people who could benefit from further testing. Overall, this study shows that regardless if you have Alzheimer’s or not, it is important to get enough slow-wave, deep sleep, or else you may reap the consequences later in life.

The More You Sit, The More You Forget!

Researchers from the University of California, Los Angeles recently discovered a linkage between the memory of middle to older aged adults and their sedentary behaviors, actions that require little energy like sitting or lying down.

They concluded that long periods of sitting, like at a desk chair, affects the specific region of the brain that is involved in creating new memories, the medial temporal lobe. The UCLA researchers closely studied 35 people ages 45 to 75 years old, documenting their physical activity for two weeks prior to and during the study.  After the three months of research, they used a high resolution MRI scan and quickly noticed similarities between the thickness of each adult’s medial temporal lobe who spent on average the same amount of hours sitting everyday. The more hours spent sitting, regardless of any physical activity, the more thin the medial temporal lobe. “The participants reported that they spent from 3 to 7 hours, on average, sitting per day. With every hour of sitting each day, there was an observed decrease in brain thickness, according to the study. ”

Even though the findings of this study are preliminary, it suggests that “reducing sedentary behavior may be a possible target for interventions designed to improve brain health in people at risk for Alzheimer’s disease.” Becoming more active is always a great thing, but becoming conscious of how much time you spend being inactive and working to decrease that, could help you out more than you think. There is still more research to be done on this matter but this is a step in the right direction for improving life for those with memory related diseases and improving overall brain health.

To read more check out the full article here!

New Developments in the Biology of Alzheimer’s Disease

Recent work by Boston University School of Medicine researchers shows developments in a new model for the biology of Alzheimer’s disease, which could lead to entirely new approaches in treating the disease. Alzheimer’s disease disrupts one’s cognitive abilities, including memory, thinking, and behavior. It accounts for 60-80% of all dementia cases. The neurodegenerative disease is caused by clumps and accumulations of 2 proteins –beta-amyloid and tau– which cause nerve cell injury and in turn, dementia.

Comparison of a normal brain (left) and the brain of a person diagnosed with Alzheimer’s (right).

Recent work by the BUSM researchers has shown that the clumping and accumulation of the tau protein are largely due to stress. The accumulation of tau produces “stress granules” (RNA/protein complexes). The brain responds to these stress granules by producing important protective proteins. However, with excessive stress, there is a greater accumulation of stress granules, which in turn leads to greater accumulation of clumped tau, which causes nerve cell injury. In this study, researchers are using this model to show that reducing the level of stress granules could lead to improved nerve cell health. It may be possible to reduce the level of stress granules by genetically decreasing TIA1, a protein required for stress granule formation.

In an experimental model of Alzheimer’s disease, the research team found that reducing the TIA1 protein led to striking improvements in memory and life expectancy. However, although stress granule levels decreased (leading to better protection), the team observed that the clumps of tau became larger. The researchers further looked at the tau pathology and found that the while small clumps of tau (known as tau oligomers) are toxic, larger tau clumps are generally less toxic. According to pharmacology and experimental therapeutics professor Benjamin Wolozin, this discovery would explain why the experimental models experienced better memory and longer life expectancy. The implications and ability of TIA1 protein reduction in order to provide protection may lead to further novel developments in the biology and treatment of Alzheimer’s disease.

Source: https://www.sciencedaily.com/releases/2017/11/171120111319.htm

Taking care of your gut might be a pain now, but is definitely worth it!

Brain with Alzheimer’s

The contributions of microbes to multiple aspects of human physiology and neurobiology in health and disease have up until now not been fully appreciated.
Many people have said the human gut is like a “second brain.” With trillions of microbes, the digestive tract of the human gut can influence many things such as your metabolism, nutrition, immune function, and even your happiness. New research continues to show links between the brain and the health of the gut.

For example, a study from Lund University found that “unhealthy intestinal flora can accelerate the development of Alzheimer’s disease.” Alzheimer’s disease is an extremely common form of dementia or memory loss. It is caused by the death of many brain cells, which progressively decreases the size of the brain and the number nerve cells and connections. This study showed that mice with Alzheimer’s have a different bacterial profile in their guts than mice without this disease. Dr. Frida Fak Hallenius said that “Alzheimer’s is a preventable disease and in the near future we will likely be able to give advice on what to eat to prevent it. Take care of your gut bacteria, by eating lots of whole-grains, fruits and vegetables.”

 

After these discoveries, researchers are looking deeper into how bacteria can affect brain pathology. One of their ideas is that the bacteria may affect T-cells in the gut, which controls inflammatory processes both in the gut and brain. Therefore, if we can find a way to increase the health of the gut, we can reduce inflammation and brain damage. Alzheimer’s, while it is one of the most feared diseases, is preventable to in extent and if not preventable, there are several ways to delay it. The human gut microbiome has a huge impact on your health and your brain’s health. If scientists can continue to discover how to make your gut as healthy as possible, Alzheimer’s could soon be a thing of the past.

http://www.huffingtonpost.com/entry/gut-bacteria-alzheimers_us_589e0e09e4b03df370d628be

http://www.nature.com/news/the-tantalizing-links-between-gut-microbes-and-the-brain-1.18557

Can Probiotics Cure Alzheimer’s?

 

 

Research on how gut microbiota affects Alzheimer’s Disease, also called AD, has been done, and promising data collected. The only problem is that all of this data comes solely from research done on mice. There has been minimal research up to the present that was tested on actual people.

The closest thing to real-life research in this field, however, would be the research done by Dr. Mahmoud Salami, as reviewed by Gut Microbiota Research and Practice. Dr. Salami has collected data from a trial he is conducting in Iran. This trial consists of 60 people between the age 60 and 95. Now since we know that there has been minimal research on how gut microbiota effects Alzheimer’s, this work done by Dr. Salami is impressive.

Dr. Salami has found that a daily dose of probiotic Lactobacillus and Bifidobacterium bacteria taken over 12 weeks may improve cognitive function in elderly Alzheimer’s patients. Although more research must be done to have more definitive answers, Dr. Salami’s research opens up even more of a reason to human testing to be done.

Countless research has been done on how where one lives can affect there health, so wouldn’t it be interesting to see if data, similar to Dr. Salami’s, collected in varying locations throughout the world may provide varying results due to the location the participant calls their home?

 

 

Could drinking milk reverse the effects of Alzheimer’s?

While it may seem like a stretch, researchers have recently discovered a link between probiotics, or good bacteria, in our intestinal tracts and neurological function. A study done at Kashan University of Medical Sciences and Azad University in Iran has revealed that probiotics can improve cognition in those suffering with Alzheimer’s.

Many studies done in the past have shown that probiotics in mice have resulted in improved memory and learning as well as reduced depression, anxiety and OCD- related behaviors. These surprising findings have led scientists to be curious about weather or not humans would benefit in the same ways. Prior to this most recent study however, no research has been done on the effects of probiotics in human brains.

 

52 men and women between 60 and 95 years old with Alzheimer’s participated in this groundbreaking study. Half of the participants were randomly chosen to receive 200 ml of milk enriched with probiotic bacteria, while the other half were given untreated milk daily for 12 weeks. Prior to beginning the study, participants and were given a questionnaire testing cognitive function, which included tasks like repeating a phrase, giving the current date and naming objects. While these may seem like simple tasks to us, patients suffering with Alzheimer’s have great difficulty completing such actions.

 

Over the course of the 12-week study, the participants were repeatedly given the same questionnaire. The scores of the group who received the enriched milk increase significantly, averaging from an initial 8.7 increasing to 10.6 out of 30, while the scores of the group that received the un-enriched milk mostly remained the same or decreased.

 

While this area of research is still in its primary stages, the findings of this study helped us discover an important connection between the gastrointestinal tract and neurological function, as well as how probiotics have a direct effect on cognition. Researchers have hope that further study can reveal more about the affects of probiotic on Alzheimer’s and other neurological conditions.

Probiotics: The Real Brain Food

While it is nearly common knowledge that probiotics give partial protection against certain colds, allergies, infectious diarrheas, and other health issues, scientists were not able to prove until recently that probiotics can potentially improve cognition. This is possible since there is communication between the gastrointestinal tract and the brain via the nervous system, the immune system, and hormones.

Scientists have seen that in mice, probiotics have caused an improvement in learning and memory. Researchers from Kashan University of Medical Sciences, Kashan, and Islamic Azad University, Tehran, Iran, completed a double-blind experiment where 52 men and women with Alzheimers (between 60 and 95 years old) either received milk enriched with four probiotic bacteria, or untreated milk. As predicted by several researchers, by the end of the 12 week period, those who received the milk with Lactobacillus acidophilus, L. casei, L. fermentum, and Bifidobacterium Bifidum displayed an improvement in cognition. To determine these results of the study, the scientists asked the participants of the study to complete tasks such as giving the current date, repeating a phrase, and counting backwards from 100 by sevens. Those who received the probiotics earned a “score” on these tasks ranging from 8.7 to 10.6 on the scale out of 30, whereas the participants who did not receive the probiotics scored slightly lower ranging from 8.5 to 8.0. Despite the seemingly minute difference, these results provide scientists with an insight as to the fact that probiotics can improve human cognition.

alzheimers_disease_brain_comparison

In the near future, scientists hope to test these results based on longevity of their intake to test whether or not the effects of probiotics grows throughout prolonged treatment. The patients who received the probiotics also demonstrated lower levels of triglyceride, Very Loy Density Lipoprotein (VLDL), high sensitivity C-Reactive protein (hs-CRP) in the blood of the Alzheimer patients, and a reduction in two common measures of insulin resistance and the activity of the insulin-producing cells in the pancreas. These results also signify that this change in metabolic adjustments might be a way that the probiotics impacts other cognitive and neurological disorders.

Further Reading:

http://www.medicalnewstoday.com/articles/314044.php

http://www.express.co.uk/life-style/health/731021/yoghurt-Alzheimers-symptoms-improve

If You Didn’t Already Know, You Shouldn’t Eat Sharks

Can sharks give you Alzheimer’s disease? Do people actually eat sharks?

screen-shot-2016-11-14-at-12-47-10-pm

NOAA, national ocean service image gallery flicker.com/photos Licensed for reuse/public domain

The answer to both of these questions is yes. A recent study by the university of Miami found large amounts of toxins that are linked to brain disease. It has been recently found that about 10 types of sharks have high concentrations of these toxins and that the consumption of these sharks can actually lead to the development of brain diseases such as Alzheimer’s. Though it is very uncommon for someone to be found eating a shark in the U.S, shark is widely consumed across Asia so many asians may be at risk of developing brain diseases. The shark population is rapidly decreasing due for the desire to have shark fin soup, a delicacy across Asia, and this new information may be used to help the argument against the killing of sharks. Since sharks are becoming more and more endangered, this discovery could help save the lives of sharks and of people. So people, especially ones that consume shark, must learn that eating shark can have real negative effects on peoples lives and by killing sharks they are helping the endangerment of the species. This killing and consuming of sharks needs to stop to help save sharks and people.

Hammer Head Shark 1893 No Known copyright restrictions flicker.com/photos

Hammer Head Shark
1893
No Known copyright restrictions
flicker.com/photos

Lead Leads to Neurotoxitity

Have you ever heard of using bottled water to shower? Sounds ridiculous right, but the people of Flint, Michigan need to do this to save their lives. The city of Flint switched their water supply from Lake Huron to the Flint River in April 2014. The river was later discovered to be contaminated. Since the changeover, scientists have linked the high lead levels in children’s blood to the contaminated water. This is a serious problem.

Lead is a highly toxic substance that permanently affects humans’ brains by killing nerve cells. Not only does lead harm kids’ brain processes, it also may cause various future mental diseases, such as Alzheimer’s disease and Schizophrenia. Throughout U.S. history, people have been exposed to lead poisoning through basic everyday mediums, such as paint, water (from lead-contaminated water pipes), and dust. Children who eat paint chips or lick their fingers after coming in contact with products that have a lead component are poisoning themselves. The lead enters into the bloodstream and travels throughout the body, stealthily making itself at home, poisoning the body.

So how does lead poisoning work? Basically, lead disguises itself as zinc. Zinc is needed to anchor proteins that switch genes on and off. When zinc is replaced with lead, the switches cannot function properly, eventually leading to mental diseases.

Lead Poisoning

Scientists have been researching the possibility that lead is transferable in DNA to offspring. This could be devastating to a population of a town like Flint, Michigan, where the mothers who have lead poisoning could pass this on to their babies. The worst part is that there is no cure for lead poisoning.

Because of the devastating effects of lead in bloodstream, governments have debated the topic of legalizing contaminated water as a bioweapon, using lead as the contaminant. Governments in the past have used poisoned water as an assassination method, proving the effectiveness of this strategy.

Preventing lead exposure and poisoning is critical for children’s health and for future generations.

 

Source Article

For more info on the biowarfare, click here.

Could There be Good Gene Mutations?

Is there an epic battle occurring within our bodies right now? The classic battle royale between good and bad? I suppose in the body’s case the fight between good and bad genes.  There is a new field in medical research in which researchers are on the quest to find good gene mutations that fight against the disease causing mutations.  One individual, Doug Whitney, sparked the interest of a few doctors because he has fought his genetic odds to be health at 65 years old.  Whitney has a gene mutation, presenilin, that causes early onset Alzheimer’s disease in those who has inherited it. Whitney’s mother and 9 out of his 13 siblings were killed by this mutation and so Whitney’s fate seemed to be sealed.  However when Whitney reached his 40s and 50s having no symptoms he assumed he did not have the gene.  At 62 years old, Whitney, decided he would get a gene test.  He did have the gene.  This was an anomaly, He was doomed to have early onset Alzheimer’s Disease but had absolutely no symptoms. Although Whitney still have changes of getting Alzhiemers but the effects of his bad gene have been greatly delayed by another gene in Whitney’s DNA.  Whitney joined a study at Washington University in St. Louis led by Doctor Randall Bateman which recruited people with the early onset Alzheimer’s disease gene. This attracted the attention of Doctor Eric E. Schadt and Doctor Stephen H. Friend.  Doctor Schadt said that searching for good genes that protect against bad gene mutations is completely turning genetic research on its head.  Researchers have found gene mutations that partially protect diseases like osteoporosis, Type 2 diabetes, heart disease, and Alzheimer’s.  These good gene mutation’s partial protect have help to develop drugs to help fight certain diseases. Finding good gene mutations are substantially more difficult to find than bad genes, but the search has gotten a little easier with fast and inexpensive methods of sequencing DNA. Doctor Schadt and Doctor Friend decided to start the Resilience Project and search for good gene mutations that counteract bad gene mutations to help develop new break though treatments and drugs. They have contacted the researchers at Washington University, the research that Whitney is currently participating in.

For more information:

Article from NYT

Prokaryotic positive genetic influences

Genetics used for intrusion protection

About genetic testing

 

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