AP Biology class blog for discussing current research in Biology

Tag: Dementia

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.

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.


Petri Dish Brain Models…Endless Possibilities.

Side View of the Brain

Who would have thought that modern science could develope a brain stimulation with actual brain cells in a petri dish? Well researchers led by Doctor Rudolph E. Tanzi have done just that.  They have made substantial steps in the field of medical brain research specifically in the Alzheimer’s research field. Rudolph E. Tanzi is a prominent neuroscientist at Massachusetts General Hospital in Boston. One of Tanzi’s colleagues and also a neuroscientist, Doo Yeon Kim, suggested that they grow brain cells in gel. From this suggestion researchers under Tanzi’s lead created a brain scenario in a petri dish and then gave this model Alzheimer’s disease. Tanzi and his group took embryonic stem cells, which have the potential to become any type of cell in the body, and grew them with a mixture of chemicals. Said chemicals cause the stems cells to become neurons, which they then gave those neurons Alzheimer’s genes and were all growing in a commercially available gel in a petri dish. Those genes then caused plaques and later tangles which are indicative characteristics of Alzheimers. Dr Tanzi was quoted, “Sure enough, we saw plaques, real plaques…We waited, and then we saw tangles, actual tangles. It looks like you are looking at an Alzheimer brain.” This manufactured real Alzheimer’s brain stimulation opens new doors for research that was hindered because previously on mice with imperfect formsof the human Alzheimer’s genes. Doctor P. Murali Doraiswamy of Duke University states, “It could dramatically accelerate testing of new drug candidates.” Although the Petri Dish Model lacks some real life qualities it can still be utilized as a start for quick, cheap, and easy drug testing. Doctor Sam Gandy of the Icahn School of Medicine at Mount Sinai in New York states that the new discovery is, “a real game changer.” Tanzi is now starting to test 1,200 drugs on the market and 5,000 experimental drugs, a project that was impossible to perform on mice. Tanzi also wishes to test a protein, amyloid, that clumps into the plaques. He found an enzyme, that when blocked prevents tangles from forming. Dr. Gandy wishes to use the the system to study the influence of genes, such as ApoE4, which contributes to about 50% of Alzheimer’s cases. Dr. Doraiswamy of Duke stated, “The lack of a viable model for Alzheimer’s has been the Achilles’ heel of the field.” Tanzi’s model is the first step towards defeating this “Achilles’ heel” which opens infinite new doors in the research of finding new medications to cope with the devastation of Alzheimer’s disease.

For more Information: 

Official Alzheimer’s Research Page

Neuroscience Research 

Actual Article




Don’t forget your sleep

Photo Credit: Me

Let’s face it there are many nights when we don’t get the sleep we need for some reason or other.  Not getting the recommended eight hours of sleep is pretty much the norm for students, but according to a new study this lack of sleep could really be hurting us later on.  This new study found that disrupted sleep appears to be associated with the build-up of amyloid plaques, which are a known to be a hallmarks of Alzheimer’s disease, in the brains of people who did not yet have any memory problems.

The author of the study Yo-El Ju, who works with Washington University School of Medicine conducted the study by testing the sleep patterns of one hundred people, ages 45 to 80, who were free of dementia.  Half of this group had a family history of Alzheimer’s.  Sleep diaries and questionnaires were used to learn about the patients sleeping habits as well as a device placed on the participants for two weeks to measure sleep.

The study found that 25% of the participants had evidence of amyloid plaques, which are known to be able to show up years before symptoms of Alzheimer’s appear.  Most of these people spend an average of eight hours in bed, but only 6.5 hours asleep due to waking up at night.  The study found that people who were waking up more than five times an hour were more likely to have the amyloid plaque build-up than the people who didn’t wake up much at all.  The study also said that people who slept less efficiently were more likely to have markers of early stage Alzheimer’s disease.  Dr.Ju says it will take more time and data to fully understand the link, but I think for now it is safe to say that sometimes we should put our homework down and get to sleep.

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