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Good News for Sufferers of Alzheimer’s disease

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FDA approves two new treatment medications

Two new types of Alzheimer’s treatment medication have been recently approved by the FDA. The new drugs are memantine and cholinesterase inhibitors. Both work on cognitive dysfunction, which is one of the most debilitating outcomes of the disease.

Alzheimer’s disease and cognitive function

One of the consequences of Alzheimer’s is that brain cells die and the connectors, or synapses, between cells become more damaged as the disease progresses, triggering worsening cognitive functioning. The patient’s ability to learn and remember is severely hampered. Medications currently available are not able to reverse the damage caused by Alzheimer’s, although they do offer hope for calming the symptoms.

Memantine and cholinesterase inhibitors work on the neurotransmitters

Neurotransmitters help neurons communicate. Alzheimer’s disease hinders this process by damaging the synapses. The new drugs address this problem in different ways. Memantine regulates glutamate, a key neurotransmitter that impacts learning and memory. If glutamate attaches to the surface of cells, calcium can enter. When Alzheimer’s disease is present, the amount of calcium that enters the cell reaches a level that intensifies the cell damage. Memantine works to decrease the calcium entering the cell. Cholinesterase inhibitors slow down the process whereby key neurotransmitters are damaged.

Typical Alzheimer’s disease treatment methodology

A treatment protocol is established for the Alzheimer’s patient by the doctor depending upon a number of factors. These include:
• The patient’s medical history and current health assessment
• How far the disease has progressed
• The patient’s ability to tolerate medicines and treatment therapies
• Prognosis for the future
• Preferences of the patient and/or guardians

Clinical trials

The only way to determine the effectiveness of new treatment medications is to safely introduce the drugs to people and then document the outcomes. Clinical trials involve a carefully regulated application of new drugs to patients which yields invaluable answers to the questions of a drug’s effectiveness. It is the paramount way for researchers to develop new drug therapies that can reverse, or at least halt, the ravaging effect of Alzheimer’s, and ultimately prevent the disease from occurring.


Seeking the Source of Alzheimer’s Disease with Ground Breaking Study

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Synapse in brainThe 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.

New Drug Offers Hope for Stemming Memory Loss in Alzheimer’s Patients

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Dr. Martin Watterson, John G. Searle Professor of Molecular Biology and Biochemistry at Northwestern University Feinberg School of Medicine, is the lead author of research findings that offer a tremendous glimmer of hope for Alzheimer’s patients. He has announced the discovery of new molecules that work in a drug-like fashion to target brain enzymes that contribute to early memory loss in Alzheimer’s patients. These molecules, developed in the laboratory of Dr. Watterson, have been observed to not only halt memory deterioration but also to repair communication in the brain cells of mice.

Scientists note that changes in brain structure begin as much as ten to 15 years before the symptoms of memory loss are visible. Dr. Watterson hopes that in the future a new class of drugs can be developed from these enzymes that will be administered at sufficiently early stages, when nerve cells are just beginning to become damaged, and thereby halt certain aspects of memory loss in Alzheimer’s.

One of the causes of the brain inflammation and impaired neuron functioning that we see in Alzheimer’s is due to the enzyme p38 mitogen-activated protein kinase (p38MAPK) that becomes over-active in the brains of Alzheimer’s patients. This new drug-like molecule, named MW108, may inhibit the toxic impact of p38MAPK in the brain. In mice trials, researchers discovered that MW108 inhibited the release of inflammatory proteins, as well as served as a shield against the damaging effects of beta-amyloid. When injecting MW108 into mice before delivering beta-amyloid into their brains, the mice continued to perform well on memory and learning tests.

With such stunning results, researchers are optimistic over the possibilities of developing novel drug therapies that specifically target molecular processing in the brain. Additionally, scientists now have a new strategy for cultivating novel drug therapies that address other aspects of Alzheimer’s as well as other neurological diseases. Through funding from the National Institutes of Health, Dr. Watterson and his team will work to further stabilize MW108 so that researchers can safely move into phase 1 clinical trials on humans.

Manipulation of Reelin signaling offers hope for reversing cognitive function of Alzheimer’s patients

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Neurofibrillary Tangles
Neurofibrillary Tangles

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.

New Findings Suggest that Zinc is key factor in Enzyme that Regulates Cell Death

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New findings by Virginia Commonwealth University (VCU) researchers implicate naturally occurring zinc as a causative agent in regulation of apoptosis. This is a significant development in the search for drug therapies to treat debilitating illnesses and diseases such as cancers, Parkinson’s and Alzheimer’s.

The VCU research findings were recently published in Angewandte Chemie, in its international edition. Apoptosis is the naturally occurring process of cell death. There are a number of enzymes that regulate the process of apoptosis. If there is a deficiency in one of the mechanisms regulating apoptosis, neurological diseases such as Alzheimer’s occur. It has been established that zinc inhibits caspase activity, thereby regulating apoptosis. Drug treatments in use today for cancer and Alzheimer’s target the caspases, therefore this new research could be key to the scientific discovery of new therapeutic agents.

Eleven caspases are identified today. Researchers focused their efforts on caspase-3, one of the seven caspases known to regulate apoptosis. Using established biophysical and enzymologic techniques, they discovered a heretofore unknown interaction between zinc and caspase-3. Nicholas P. Farrell, PhD. of the VCU Developmental Therapeutics program said that further study will need to be conducted, but it could be that zinc is interacting with all the caspases. If so, then the focus will be on developing drug therapies that would target this zinc-caspase interaction to regulate apoptosis.

In the meantime, the study is precipitating a new line of scientific inquiry, called bioinorganic chemistry of apoptosis, which is examining and seeking to understand how the requisite metal ions are interacting in the fundamental process of life and death of cells. Dr. Farrell noted that zinc’s role in constraining apoptosis is exactly the opposite of the metal closest to it—copper, which is known to accelerate apoptosis. 

Michael Mullan: Sex Differences in Alzheimer’s Disease

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Illustration to go with the review of the book, "Brainstorm: The Flaws in the Science of Sex Differences" by Rebecca Jordan-Young
Illustration to go with the review of the book, “Brainstorm: The Flaws in the Science of Sex Differences” by Rebecca Jordan-Young

Article Written by Dr. Michael Mullan

There has long been controversy over whether women or men are most affected by Alzheimer’s disease. Decades ago the perceived wisdom was that Alzheimer’s affected women more than men because women live longer than men and Alzheimer’s is a disease of aging. However, this apparent sex discrimination was challenged in subsequent studies and more recent investigations suggest that women may be at greater risk than men on an age matched basis. However, even this is controversial and may differ between populations.

For instance, some American studies report equal rates between men and women whereas European ones report a sex difference with more women than men being affected. However, several incidence studies looking at new cases of Alzheimer’s suggests that women are more readily affected than men.

Many reasons have been offered as to why there may be sex discrimination by Alzheimer pathology. One idea is that loss of sex hormones after menopause is particularly detrimental to the human brain. It’s known, for instance, that sex hormones can regulate Beta amyloid production. Cell culture studies show that estrogen and testosterone can mitigate the production of amyloid, one of the central features of Alzheimer’s.

Sex hormones may play other roles as well as regulating the amount of amyloid produced. They may have a role for instance in the breakdown of amyloid and the clearance of amyloid by other mechanisms in the brain. It’s also possible that progesterone have a protective role in the brain. Evidence suggests that after difference insults to the brain, progesterone can be protective.

While all of these observations on the sex differences have been very valuable, no therapy has yet emerged based on hormone replacement. In fact, key studies looking at hormone replacement in post-menapausal women have not shown any beneficial reduction in the risk for Alzheimer’s disease. At best, hormone replacement therapy has shown mixed results in relation to any protection against Alzheimer’s disease. Interestingly, any evidence that sex hormones are helpful in Alzheimer’s are restricted to prevention strategies rather than treatment strategies. In other words, it looks as if prolonged exposure to sex hormones may influence the rate of Alzheimer’s disease; but, once the disease is established, sex hormone therapy is not clearly protective.
So, although there is evidence that Alzheimer’s disease does indeed discriminate against women, the underlying causes are still uncertain and simple hormone replacement therapy may not be the best answer. However, more broadly, Alzheimer’s discriminates against both genders once natural hormone levels start to fall in the later decades of life.

Much more work needs to be done to understand these effects and to ask whether any of these findings can be turned into new clinical treatments for the disease.

Michael Mullan – A leader in Alzheimer’s disease research

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Michael MullanDr. 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 institute

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.