40 Days of Glow: Day 17 – Alzheimer’s and Mitochondrial Disease
What is the role of mitochondrial dysfunction in Alzheimer’s disease?
Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role in the cause of Alzheimer’s disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics, and degradation by mitophagy occur during the disease process, contributing to the onset and progression of Alzheimer’s disease.
Mitochondrial abnormalities correlate with some of the structural changes that are seen in brains of Alzheimer’s patients. Age-related degradation of mitochondria function is a prime suspect in the pathophysiology of sporadic Alzheimer’s disease.
Treatment and Research:
Currently, there is no cure for Alzheimer’s disease. However, treatments, such as cholinesterase inhibitors and glutamate regulators, are often successful is slowing the rate of progression of the disease. So early diagnosis of Alzheimer’s would enable treatment to begin early, when it could be most beneficial.
Recent research may prove to be helpful in early diagnosis. Researchers at the Mayo Clinic recently published a paper8 showing that mitochondria in the brain are dysfunctional early in the disease – even before symptoms appear. Connecting the degree of mitochondrial dysfunction with the progression of symptoms of Alzheimer’s disease will be useful not only to diagnosis the disease, but could also provide new treatment targets, and can be used to help monitor the progression of the disease. The research was performed in mice, but the researchers expect to validate the changes in humans with the disease. Researchers are also actively researching new targets for Alzheimer’s disease treatment as well as new therapies. It is recognized that successfully treating Alzheimer’s disease will likely include treatments aimed at correcting the mitochondrial dysfunction component of the disease.
Deep Brain Stimulation Shows Promise Against Alzheimer’s Disease
A German study using deep brain stimulation on patients, a treatment that can be used for patients suffering from Parkinson’s disease, showed some promise, with 4 out of 6 patients responding to treatment.
Deep brain stimulation is a procedure in which a brain pacemaker is implanted in the brain to send electrical impulses to specific parts of the brain. In the case of Alzheimer’s disease, the electrical impulses are sent to a region of the brain associated with the ability to think clearly and efficiently.
The use of deep brain stimulation as a treatment for Alzheimer’s disease is a relatively new idea. Despite the fact that 33% of seniors die with some form of Alzheimer’s or dementia, there is a startling lack of treatments in reversing the memory loss associated with these diseases. The German study provides hope for those suffering from this disease has opened doors for the improvement of the stimulators used for deep brain stimulation.
The Functional Neuromodulation study group announced last week that it had found 42 Alzheimer’s disease patients in the United States and Canada to study as a result of the success of the German study.
Due to the lack of a control group in the initial German study, the study by Functional Neuromodulation plans to specify what works and what doesn’t about the use of deep brain stimulation as a treatment option for Alzheimer’s disease patients.
Click here to learn more about the relationship between Alzheimer’s disease and mitochondrial dysfunction.
Researchers Fight for Alzheimer’s Cure
Alzheimer’s disease is the nation’s sixth leading cause of death and is predicted to affect 15 million elderly Americans by 2050.
Charles DeCarli is a neurologist and Alzheimer’s Disease Center director at UC Davis. Their clinic sees both patients and research study participants. They use a wide variety of treatments to attempt to stymie the damage this disease causes to the brain. The damage Alzheimer’s disease causes to the brain are startling.
According to Alz.org, brain atrophy is a prominent symptom in those affect. Parts of the brain that deal with memory and thought formation shrink, while fluid-filled spaces of the brain become larger.
DeCarli prescribes medications like Aricept and Nemenda, medications specifically geared to slowly memory loss in dementia associated with Alzheimer’s disease. However, the clinic is focusing on alternative methods of treatment to slow memory loss. Their clinic offers classes like Brain Fitness 101 to offer treatments emphasizing a healthy diet and brain exercises that can only postpone the decline in cognition.
The recent recession caused California, already the nation’s leader in researching Alzheimer’s disease, to cut funding to centers like the one DeCarli works. Despite the fact Alzheimer’s disease or other forms of dementia affect 1 in 3 seniors funding for this disease pales in comparison to diseases like cancer. Cancer researchers receive about $5 billion by the federal government each year, while Alzheimer’s researchers receive about $560 million.
DeCarli evaluates the research participants on a monthly basis, attempting to identify patterns in his patients’ deterioration. One of the more difficult parts of dealing with Alzheimer’s is noting the stages it attacks the brain. Working against a limited budget and time, his clinic uses autopsies of patients in an attempt to make sense of the way it affects research participants.
Alzheimer’s research is still greatly underfunded. You can make a difference by donating today.
What is the role of mitochondrial dysfunction in Alzheimer’s disease?
Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses associated with the etiology and underlying disease components of Alzheimer’s disease.2 Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role in the cause of Alzheimer’s disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to the onset and progression of Alzheimer’s disease.
FMM Celebrated Brain Awareness Week
Brain Awareness Week (BAW), which was March 10-16, is really being celebrated all month. It is the global campaign to increase public awareness of the progress and benefits of brain research. From child development to healthy aging, brain awareness shows how the newest developments in neuroscience can affect – and improve – our lives.
The Foundation for Mitochondrial Medicine’s Web of Connectivity includes diseases like Parkinson’s, Alzheimer’s, and Huntington’s, all three diseases of the brain. In honor of Brain Awareness Week, check out this blog about the brain. Find information regarding diseases, structures, and facts about the brain to learn more.
MRIs are being used to identify areas of the brain of the patients suffering from neurological symptoms. Scientists from the University of Montreal found the thinning in the grey matter correlates to cognitive issues in these patients. This is believed to be an indicator of the early stages of dementia, disease with strong links to Parkinson’s.
For the first time, scientists at Georgetown University have developed a blood test that can predict, with great accuracy, whether someone will develop Alzheimer’s disease. The test could someday help researchers develop drugs for the degenerative brain disorder. Early detection is key to better management and quality of life for patients who suffer from this disease.
Whether March for you means basketball or changing clocks, we hope you will check out some of the Brain Awareness events.
To learn more about mitochondrial diseases related to the brain, visit hopeflies.org.
If Alzheimer’s disease were a national economy it would rank #17
Reports continue to highlight Alzheimer’s disease as a priority for our nation and the world. As Dr. Murali Doraiswamy, M.D., of the Duke University Institute for Brain Sciences described during the 2014 World Economic Forum in Davos, Switzerland, Alzheimer’s represents an enormous threat to public health.
With the numbers and costs of people impacted by Alzheimer’s rising, so becomes the importance of finding connections among related neurodegenerative diseases, from early childhood genetic diseases to late life diseases, such as Alzheimer’s disease or Parkinson’s disease. If you know someone affected by Alzheimer’s, then you know someone connected to mitochondrial disease.
The Foundation for Mitochondrial Medicine is funding research that will impact both of these diseases. Check out FMM’s recent award to Dr. James Bennett, of Virginia Commonwealth University. FMM’s collaborative strategy to co-fund treatment research with related disease groups, such as the Alzheimer’s Drug Discovery Foundation, means research dollars go farther and thus, the potential exists for the rising tide to lift multiple boats.
Mitochondrial dysfunction has surfaced as one of the most discussed hypotheses acting as a trigger for the pathogenesis of Alzheimer’s disease. Mitochondria assume central functions in the cell, including ATP production, calcium homeostasis, reactive oxygen species generation, and apoptotic signaling. Although their role as the cause of the disease may be controversial, there is no doubt that mitochondrial dysfunction, abnormal mitochondrial dynamics and degradation by mitophagy occur during the disease process, contributing to its onset and progression.
Click here to learn more about the relationship between Alzheimer’s and mitochondrial dysfunction.
Alzheimer’s Drug Discovery Foundation and Foundation for Mitochondrial Medicine Partner to Support Novel Research for Mitochondrial-Directed Therapies
Research could lead to development of new therapies to treat a variety of mitochondrial diseases, including Autism, Alzheimer’s, Parkinson’s and Lou Gehrig’s disease
ATLANTA and NEW YORK, February 26, 2014 – The Alzheimer’s Drug Discovery Foundation (ADDF) and the Foundation for Mitochondrial Medicine (FMM) announced today that they have awarded $200,000 in funding to James Bennett, M.D, Ph.D. to further research gene therapy of mitochondrial protein in the brains of mice with experimental Alzheimer’s disease. Bennett is studying rhTFAM, a novel human mitochondrial protein shown to increase mitochondrial function in cell and animal models. The protein has shown to restore memory function of aged mice while increasing mitochondrial function in brains, suggesting it has great potential to do the same in humans with impaired cognition and early Alzheimer’s disease.
rhTFAM was invented and is being developed commercially by Gencia Corporation, located in Charlottesville, Va. Bennett’s research will provide critical data to support the use of rhTFAM in the use of humans.
Mitochondria dysfunction underlies many different diseases. The brain is particularly vulnerable to changes in energy use that occur with age or because of underlying disease pathology. Previous research has shown that mitochondrial in the brain are dysfunctional in early stage of Alzheimer’s, and these changes contribute to the later loss of mitochondrial function and the onset and progression of the disease.
“Novel therapies that can correct defects in mitochondria functioning have the potential to impact many different diseases,” said Bennett. “Thanks to funding support from ADDF and FMM, I’m able to continue my research into one of these novel therapies and determine possible implications for its use in a variety of areas, from early childhood genetic diseases to late-life neurodegenerative diseases such as Alzheimer’s.”
“We are delighted to support Dr. Bennett’s research involving the rhTFAM mitochondrial protein and the potential it has to impact the progression of Alzheimer’s disease,” said Diana Shineman, Ph.D., director of Scientific Affairs for ADDF. “The translational nature of Dr. Bennett’s research could have critical applications beyond Alzheimer’s disease to other related disorders that affect millions of Americans.”
“We are pleased to partner with ADDF and ensure that Dr. Bennett’s innovative, translation research is conducted,” said Laura Stanley, executive director of FMM. “Our mission is to fund the most promising treatments for the many forms of mitochondrial disease. Research like Dr. Bennett’s can unlock potential cures for many related diseases, including Alzheimer’s disease, Autism, Parkinson’s disease and others.”
Bennett holds the Bemiss Chair and is founding director of the Virginia Commonwealth University Parkinson’s and Movement Disorders Center. Bennett has held several individual NIH grants and has led two multi-investigator NIH Programs. He oversaw projects and directed the NIH-funded University of Virginia Udall Parkinson’s Research Center of Excellence for ten years. He has over 140 peer-reviewed publications that have encompassed Parkinson’s pharmacology and mitochondrial mechanisms of neurodegeneration. He has held multiple Investigational New Drug (IND) applications and is the inventor of worldwide patents involving use of a novel neuroprotective drug. His current research involves the molecular biology and pharmacology of mitochondrial dysfunction in neurodegenerative diseases, such as Alzheimer’s, Parkinson’s and Lou Gehrig’s diseases (amyotrophic lateral sclerosis). He graduated from the University of Florida in 1970 with a BS in Chemistry (with Honors). He attended Johns Hopkins University Medical School and received his M.D. degree in 1974 and Ph.D. in Pharmacology in 1977.
About the Alzheimer’s Drug Discovery Foundation (ADDF): The mission of the ADDF is to accelerate the discovery of drugs to prevent, treat and cure Alzheimer’s diseases, related dementias and cognitive aging. The ADDF has granted more than $65 million to fund nearly 450 Alzheimer’s drug discovery programs in academic centers and biotechnology companies in 18 countries. For more information, visit www.AlzDiscovery.org.
About the Foundation for Mitochondrial Medicine (FMM): The Foundation for Mitochondrial Medicine’s mission is to support the development of the most promising research and treatments for the many forms of mitochondrial disease. Cures for mitochondrial diseases could impact cures for Autism, Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease among others. For more information on FMM funded research such as functional MRI studies on cognitive fatigue and testing of new drug compounds, visit www.mitochondrialdiseases.org
About VCU and the VCU Medical Center: Virginia Commonwealth University is a major, urban public research university with national and international rankings in sponsored research. Located in downtown Richmond, VCU enrolls more than 31,000 students in 223 degree and certificate programs in the arts, sciences and humanities. Sixty-eight of the programs are unique in Virginia, many of them crossing the disciplines of VCU’s 13 schools and one college. MCV Hospitals and the health sciences schools of VCU comprise the VCU Medical Center, one of the nation’s leading academic medical centers. For more, see www.vcu.edu.
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ADDF: Michael Grela, firstname.lastname@example.org, 212.594.5500
FMM: Jennifer Grizzle, email@example.com, 770.409.1152
VCU: Frances Dumenci, firstname.lastname@example.org, 804.828.7701
Accelerating Medicines Partnership Brings New Opportunities for Drug Discovery
It is very exciting to see the latest announcement from the NIH which represents a new strategy to combine forces and funds of three significant groups: the National Institute of Health, biopharmaceutical companies and several non-profit organizations. Pilot projects will focus on three key areas: 1) Alzheimer’s disease 2) type 2 diabetes, and 3) rheumatoid arthritis and lupus. Their goal is to increase new therapies and diagnostics. We applaud the approach and are especially enthusiastic since two of the three focus areas have mitochondria as one of their core causes.
FMM is a firm believer in the cross-functional collaborative approach. In fact, our partnership with the Alzheimer’s Drug Discovery Foundation to co-fund a “Mitochondrial Drug Discovery Project,” is an example of focusing on what we have in common—the mitochondria—and pooling resources to benefit everyone. Soon, we will be announcing the recipient of the FMM-ADDF award, along with more of these types of research joint ventures.
In the name of all of those with Alzheimer’s and mitochondrial disease, join our effort. Donate at hopeflies.org
The Foundation for Mitochondrial Medicine Joins the National #GivingTuesday Movement to Fund the Cures!
The Foundation for Mitochondrial Medicine is participating in #GivingTuesday to help raise awareness about Mitochondrial Disease and other related diseases. All funds raised on #GivingTuesday will go towards the Alzheimer’s Drug Discover Foundation (ADDF) and the Foundation for Mitochondrial Medicine (FMM)’s partnership to drive innovative translational research for mitochondrial dysfunction. To learn more about this partnership, click here.
The Foundation for Mitochondrial Medicine has joined #GivingTuesday, a first of its kind effort that will harness the collective power of a unique blend of partners—charities, families, businesses and individuals— to transform how people think about, talk about and participate in the giving season. Coinciding with the Thanksgiving Holiday and the kickoff of the holiday shopping season, #GivingTuesday will inspire people to take collaborative action to improve their local communities, give back in better, smarter ways to the charities and causes they support and help create a better world. Taking place December 3,2013–the Tuesday after Thanksgiving–#GivingTuesday will harness the power of social media to create a national moment around the holidays dedicated to giving, similar to how Black Friday and Cyber Monday have become days that are,today,synonymous with holiday shopping.
To support FMM and #GivingTuesday, please donate on Tuesday, December 3, 2013!
Alzheimer’s Drug Discovery Foundation and Foundation for Mitochondrial Medicine Partner to Provide Grant for Drug Development for Novel Mitochondrial-Directed Therapies
ATLANTA, August 15, 2013 – The Alzheimer’s Drug Discover Foundation (ADDF) and the Foundation for Mitochondrial Medicine (FMM) announce a partnership to drive innovative translational research for mitochondrial dysfunction. ADDF and FMM will provide grants in the range of $100,000 to $200,000 for a one-year duration with the possibility of follow-on funding.
Mitochondria dysfunction underlies many different diseases. The brain is particularly vulnerable to changes in energy use that occur with age or because of underlying disease pathology. Novel therapies that can correct defects in mitochondria functioning have the potential to impact many different diseases – from early childhood genetic diseases to late-life neurodegenerative diseases such as Alzheimer’s disease.
Priority areas for the grant include the discovery and development of new drugs that alter mitochondria function; discovery and development of novel biomarkers of mitochondria dysfunction; validation of mitochondrial assays for drug discovery and development; and repurposing or screen existing drugs for activities related to mitochondria function.
Applications may be submitted by non-profit academic institutions and for-profit biotechnology companies, both public and private, worldwide. Funding to biotechnology companies is typically made as a program-related investment. Deadline date for applications is September 5, 2013. Submission of a Letter of Intent (LOI) is required prior to August 22, 2013.
Applications will be confidentially reviewed by the ADDF, FMM and an external Scientific Review Committee. Applications from biotechnology companies will also be reviewed by the ADDF’s external Business Advisory Board. Award winners will be publicly announced by spring 2014. All LOI and applications must be submitted electronically at www.alzdiscovery.org. For further scientific or financial aspects of proposals, please contact Diana Shineman, PhD, Director of Scientific Affairs/ADDF, email@example.com. For more information on the
application process, contact Reena Vanjani, Grants Manager/ADDF,
About the Alzheimer’s Drug Discovery Foundation (ADDF): The mission of the ADDF is to accelerate the discovery of drugs to prevent, treat and cure Alzheimer’s diseases, related dementias and cognitive aging. The ADDF has granted more than $62 million to fund nearly 415 Alzheimer’s drug discovery programs in academic centers and biotechnology companies in 18 countries. For more information, visit www.AlzDiscovery.org.
About the Foundation for Mitochondrial Medicine (FMM): The Foundation for Mitochondrial Medicine’s mission is to support the development of the most promising research and treatments for the many forms of mitochondrial disease. Cures for mitochondrial diseases could impact cures for Autism, Alzheimer’s, Parkinson’s, and Lou Gehrig’s disease among others. For more information on FMM funded research such as functional MRI studies on cognitive fatigue and testing of new drug compounds, visit
ANAVEX 2-73 linking mitochondrial functionality to Alzheimer’s
Anavex Life Sciences Corp. (“Anavex”) announces promising new data.
A press release from March 12, 2013 from PR Newswire via COMTEX announced promising data for the company’s lead drug candidate for Alzheimer’s disease. The Foundation for Mitochondrial Medicine has always been focused on fueling connections between mitochondrial disease and other related diseases, such as Alzheimer’s and Parkinson’s disease.
Mitochondrial dysfunction has been consistently reported as an early cause of Alzheimer’s disease and the treatment and cure for Alzheimer’s disease may be very connected to the cure for mitochondrial disease.
In a scientific study conducted in France at the University of Montpellier and INSERM, ANAVEX 2-73 demonstrated disease-modifying effects, including the ability to repair normal mitochondrial functionality in the hippocampus, the part of the brain involved with learning, memory and emotions.
Full Details of the Research
Mitochondrial protection in mouse hippocampus against Aß25-35 toxicity is induced by the novel tetrahydrofuran derivative ANAVEX2-73, a mixed σ1 receptor and cholinergic agonist. (PDF of study on Anavex’s website).