The question over the exact causes of Alzheimer’s disease has long been at the heart of research into the condition that affects so many of our loved ones. In a recent article by Lauren Horne, she details new research into the cause and possible treatment of Alzheimer’s disease. The study that was published in June 2014 in “Nature Medicine,” the well respected medical journal, examines the theorized effect of reactive astrocytes in the development of the disease. The study was carried out under the auspices of Drs. C. Justin Lee and Daesoo Kim in Korea and their paper was published with the title: “GABA from reactive astrocytes impairs memory in mouse models of Alzheimer’s disease.”
As described in the title of the paper, the focus of this research was centered around the effects of the reactive astrocytes. In particular, Lee and Kim pointed to the fact that these reactive astrocytes are often found in large percentages in the brains of patients with Alzheimer’s disease and are known to produce GABA, a neurotransmitter inhibitor. As they found that the reactive astrocytes were producing the GABA through Monoamine oxidase B(MAO-B), an enzyme that then passed on the GABA into the system through the BESt1 channel, they decided to target the B(MAO-B) in their testing.
What they found was that when they used the Parkinson’s disease drug Selegiline as an inhibitor to bring the levels of the GABA back to more normal numbers, they were able to succeed in slowing down the firing of neurons in the brain. In their tests that they carried out on mice with Alzheimer’s disease in the labs, those subjects who received the inhibitor treatment exhibited signs of improved memory that were consistent with their theory.
Unfortunately these results did not leave any lasting changes on the mice as the effect of the drugs wore off. However, to all those who are invested in finding a cure for Alzheimer’s disease, this study has provided valuable knowledge and new insights that may soon lead to a treatment.
Manipulation of Reelin signaling offers hope for reversing cognitive function of Alzheimer’s patients
A new study from Cell Biology Department scientists at the University of Barcelona working with laboratory mice sheds new light on the role that the protein Reelin plays in preserving plasticity in adult brains and restoring lost cognitive function. These findings were recently published in the periodical, Nature Connections, and are critical to the efforts to prevent and treat Alzheimer’s disease.
In spite of years of research seeking to locate the cause of Alzheimer’s disease, scientists still do not know the cause of this neurodegenerative ailment. However there are some known structures that appear to have a significant role in causing loss of cognitive function, neuronal death and decrease in synaptic functioning. These structures are amyloid plaques and neurofibrillary tangles. The new study reveals that when levels of Reelin were increased in the brain of laboratory mice with Alzheimer’s, cognitive loss was reversed. Further, it was confirmed that Reelin diminishes amyloid deposits and postpones the development of amyloid-beta fibril in vitro.
The role of Reelin in controlling tau protein and the amyloid precursor protein was already known, but the full extent of Reelin’s role was undiscovered. So, the researchers focused their efforts on analyzing Reelin’s role. With this new study, researchers working on prevention and treatment methodologies have a new comprehension of the bond between these two proteins and Reelin’s role in regulating them. The study proves that an increase in Reelin is beneficial to reversing the effects of Alzheimer’s disease.
Researchers discovered the nature of the interaction between Reelin in vitro and the peptide AB42, a lethal peptide responsible for the accumulation of senile plaques and formation of fibril. In vitro tests on mouse models revealed that Reelin was functioning to reduce plaque and delaying fibril formation. With these findings, researchers offer Reelin as a promoter of adult brain plasticity and protective agent for neurons. Future research will concentrate on identifying chemical composites that can stimulate Reelin signaling.
Dr. Michael Mullan is CEO of the Roskamp Institute, a Sarasota, Florida based research facility. The institute conducts research on Alzheimer’s disease and other neurodegenerative disorders, as well as traumatic brain injury aftermath and potential biological markers for substance abuse. Mullan specifically works in the Roskamp Memory Disorder Clinic, where he focuses on finding treatments, and hopefully a cure, for Alzheimer’s disease, which affects approximately 5 million Americans, mostly ages 60-80.
Mullan’s inspiration for studying Alzheimer’s
On one of his blogs, Michael Mullan discusses why he focuses on Alzheimer’s in his research. He points to the amazing history of many sufferers of the disease; they have long memories over the course of lives consisting of many interesting experiences, either in the military, in business or otherwise. One of the expressions of Alzheimer’s is that short term memory deteriorates, while older memories seem more present and clear. The tendency to nostalgia for Alzheimer’s patients, he believes, is fascinating; while the short-term memory loss causes agony for the patient, as well as their families. Mullan takes pride in the fact that he has the ability to offer these people a treatment for their disease. Although it is not yet a cure, his ability to offer FDA approved drugs and treatments, as well as experimental methods the Roskamp Institute is exploring, gives hope to many people who are suffering from their loved ones’ memory loss. Being able to give people hope in dealing with such a difficult disease, which affects the entire family, is one of Mullan’s main inspirations for continuing steadfastly in his research.
The Roskamp Institute is funded by its namesake, as well as the National Institutes of Health, the U.S. Department of Defense, the Veteran’s Administration and CTAC. Their research is not just into Alzheimer’s, however; the Memory Disorder Clinic also deals with post-trauma patients, especially those with head trauma. This is the reason for many military veterans participating in the institute’s research. Mullan and his partner, Dr. Fiona Crawford, lead a team aiming to develop therapeutic methods and specific targets to achieve a deeper understanding of Alzheimer’s and its etiology. Mullan’s team discovered a genetic error which causes an excessive production of beta-amaloid. The mutation is what forms the basis for Alzheimer’s disease; it proves that there is a genetic propensity for the disease and lead this research team to begin searching for a way of understanding its presentation. Not only is Mullan’s Roskamp team searching for potential treatments for Alzheimer’s; they hope to find a cure and potentially also find ways to treat and cure some types of cancer.
The medical training of Michael Mullan
Originally trained as a medical professional at the London University, Mullan has received many awards throughout his career. His first was the Ethel Williams Scholarship for postgraduate research; already at this early point in his career, he was focused on Alzheimer’s research, which he conducted also at the Royal Free Hospital. He also earned a PhD from London University, studying molecular genetics.