CACQDs Therapy: Potential to Prevent Neurodegenerative Diseases

A research team at the University of Texas El Paso has found that Caffeic-Acid based Carbon Quantum Dots (CACQDs) have the potential to protect neurons from severe neurodegenerative disease damage. In general, neurodegenerative disease treatments are only symptomatic, meaning that these treatments aren’t cure-oriented. Many of these disorders in their early stages can contribute to other diseases and the aggregation of amyloid-forming protein fragments, leading to plaques or fibrils in the brain. The research team observed that CACQDs are able to remove free radicals (harmful molecules contributing to disease) or prevent them from causing damage and inhibit aggregation of those fragments without causing significant side effects. 

Although not of much help in more advanced stages, this research provides important insight into curing several neurodegenerative diseases. In general, a CACQDs treatment can be effective in preventing diseases like Alzheimer’s when addressed in the early stages. Additionally, considering that CACQDs is a derivative of coffee grounds, harvesting it is also very eco-friendly.

For more information, view the news article here and the published journal article here.

A Molecule Eliminates Clumps of Amyloid Proteins Found in Alzheimer's Disease.

 

This article highlights researchers, from the University of Tokyo, who injected mice, with Alzheimer's Disease, with a small, light-activated molecule. This molecule eliminates clumps of amyloid proteins, found in Alzheimer's Disease. Alzheimer's, ultimately, destroys neurons and their connections in parts of the brain involved with memory and later affects the cerebral cortex, which is responsible for language, behavior and reasoning. This article talks more about what Alzheimer's Disease does to the brain.  Researchers, then, shined a light, using a probe, into their brains, for 30 minutes, each day, for one week. The chemical analysis of the brain tissue showed that there was a significant reduction of the amyloid protein. Human brains have also been donated to support this research in the hopes of using it on live patients, one day. 

DNA repair protein BRCA1 implicated in cognitive function and dementia

Researchers at Gladstone Institutes have found compelling new evidence of the BRCA1's involvement with cognitive function and dementia. BRCA1's known function is in DNA repair, which is why it is a key player in breast and ovarian cancer risks because a mutation would equate to flawed functioning of the gene. Researchers were shocked to find BRCA1's role in the neurons where cells do not divide. The gene typically mends double strand breaks in damaged cells so it can have this function in the brain when neurons become damaged just from intense brain activity. The cycle of damage and repair supposedly strengthens neural connections and memory. BRCA1's function in neurons was studied in mice which had lower levels of BRCA1. The mice were found to have DNA damage, memory/learning deficits and neuronal shrinkage. These symptoms are very similar Alzheimer's, so researchers also studied the BRCA1 levels in post-mortem brains of Alzheimer's patients. Not only were the BRCA1 levels reduced 60-75% from normal levels, but it was also found that amyloid-beta proteins (accumulate in Alzheimer's patients' brains) depletes BRCA1. Now, researchers are looking at whether or not an increase in BRCA1 levels can alleviate neurodegeneration and other cognitive issues in mice. 

I find this critical research in the field of genetics and neurology because it can lead us to finding answers on alleviating the symptoms of Alzheimer's, which typically causes a lot of emotional stress from a patient's loved ones. It has been unfortunate that scientists cannot stop the progression of the disease, but now it is possible for progress in this field to be made. 

BRCA1

Alzheimer's May Have Been Transmitted via Human Growth Hormone

Alzheimer's is a form of dementia that affects memory, thinking, and behavior. The human brain is composed of neurons, nerves, and many connection networks. Together, all of these parts of the brain work together like a factory. Alzheimer's prohibits the brain from acting and performing in this systematic and connected way.  Symptoms of this disease start with memory loss and confusion, and later lead to disorientation, changes in mood and behavior, unfounded suspiscions about family and friends, difficulty speaking, swallowing, and walking.

There is question as to whether there is a connection between human growth hormone and Alzheimer's transmission between humans.  Professor John Collinge noticed the relative connection as he extracted growth hormone from the pituitary gland of eight deceased patients; all of which had injected growth hormone as a child. It was found that all eight patients had contracted Creutzfeldt-Jakob Disease (CJD) via the hormone and died.  It was confirmed that none of the patients were carriers of known genes for Alzheimer's.  However, autopsies revealed that six of the eight patients had amyloid plaques, which are seen in patients with Alzheimer's.  To rule out the idea that CJD had a connection to amyloid proteins, a study was done on 116 deceased patients that died of CJD, but did not receive growth hormone. None of the deceased patients with CJD had any signs of the amyloid protein.  This meant that there was no connection between having CJD and amyloid proteins.  There was also no presence of tau tangles (proteins that are indicators of Alzheimer's).  However, researchers found that in people who died of Alzheimer's, there was presence of amyloid proteins. 

In my opinion, I believe there is an underlying connection between Alzheimer's and the human growth hormone.  In the article, it spoke of a study recently conducted that injected human amyloid brain material into the brains of mice.  This material remained dormant in the mouse's brain, but later on regained the ability to cause disease.  This shows that even though the amyloid protein remains inactive and basically "hides", it is still there and can cause disease later on in the organism's life.  I feel that this may be the case for humans.  For example in the case of the eight donors that had growth hormone extracted from their brains, they died of CJD which made it impossible to see if they contracted Alzheimer's later on in their lifetime.  Professor John Collinge definitely sparked a fire for Alzheimer's research to progress.