BY ANNELIESE MOLL
For the UAS Whalesong
The human brain is a complex organ containing roughly 100 billion neurons. In humans, the brain continues to develop until the age of 25.
Yearly, more than 3 million cases of Alzheimer’s disease are reported. Within the next few decades that number is expected to rise to over 150 million, which means that this is a disease that many of us will either suffer from or have loved ones who do. The odds of someone developing Alzheimer’s doubles every five years after that person reaches 65. It’s estimated that this form of dementia affects one in 14 people. So far majority of people who get Alzheimer’s are over 60 years old, but there have been cases reported in people as young as 19.
Interestingly enough, Dr. Alois Alzheimer reported the first case of Alzheimer’s in 1901, and even though it’s been over 100 years since then, there has been little in the way of advances towards a cure. Yes, there are treatments that are available, but more than 99% of clinical trials for Alzheimer’s drugs have failed. Despite the number of people affected by this disease, it receives a fraction of the recourses that cancer research.
Not only does Alzheimer’s take memories and other cognitive abilities, but care for those with this disease is incredibly expensive. Current estimates state that Alzheimer’s care will cost the United States $236 billion. Even though it is the sixth leading cause of death in the United States and results in more deaths than breast and prostate cancer combined.
Here is where amyloid plaques come into play. Amyloid plaques are sticky buildups that accumulate outside of neurons. Amyloid itself is a protein that is typically found throughout the body. When this protein divides incorrectly, it creates ß amyloid which is toxic to neurons within the brain. Alzheimer’s occurs when cells and cell connections die, which destroys memory and other important mental functions. People with Alzheimer’s have more of these ß amyloid plaques within their brains than healthy individuals. However, the degree of plaque buildup does not always correlate to severity of memory loss or other functions.
Current research involving mice may have helped scientists discover a new target. Mice with genes similar to those associated with increased risk of Alzheimer’s disease in humans were observed for loss of synapses, junctions between two nerve cells, in specific regions of the brain-those mostly associated with memory. The loss of synapses indicates where nerve cells are unable to conduct neurotransmitters which spark the brain’s electrical activity.
Dr. Beth Stevens of Boston Children’s Hospital has led this new research using mice to look for a potential new treatment. Throughout her career she has noticed a protein called C1q. This protein is a trigger for a series of chemical reactions that end up marking certain synapses for destruction.
By using two mouse models, which create more than enough ß amyloid and eventually develop learning and memory deficiencies as they grow older, she and a team of researchers have determined that both strains had increased levels of the C1q protein within their brain tissue. To treat the mice, they administered antibodies to block C1q, which caused the loss of synapse to cease.
Currently, Stevens and her team are continuing to monitor the mice to see if the new drug slows their cognitive decline. In order to confirm that ß amyloid is causing the C1q to malfunction normal mice were injected with a protein that could produce plaques within the brain along with being knockouts that could not produce C1q. They noted that normal mice who were exposed to the protein had a decent loss of synapses, the knockouts were fairly unaffected. It was also found that synapses were destroyed when ß amyloid was present, which suggests that the combination of the protein and the C1q are both the culprits for the destruction of synapses. However, Stevens also added that other factors that may cause malfunctions may be found in cytokines, small proteins that are very important in cell signaling and can heavily affect the behavior of other cells. However, while some potential drugs may look promising, there is still no cure and treatments, when successful, can only temporarily slow the progression of the disease.
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