Backed by the Obama administration, the Brain Activity Map (BAM) project will span a decade with the goal of determining how brain cells collectively process information.

The U.S. already has one brain-mapping initiative under way, the Human Connectome Project. Launched in 2009, the goal of the Human Connectome Project is to construct a map of the complete structural and functional neural connections in vivo within and across individuals. The BAM project would go beyond an organizational and operational map and chart brain activity at the level of individual neurons.

“We propose to record every action potential from every neuron within a circuit,” write scientists, laying the groundwork for the BAM project in the journal Neuron last year [1]. To achieve this goal the scientists will need to study the connections between thousands to millions of cells while they are still alive — not something easy to accomplish.

With approximately 100 billion neurons, the brain is by far the most complex organ known. Although there is a good deal of knowledge regarding whole-brain activity patterns and single-cell structure and function, how “circuits” or “networks” of brain cells work together in both normal and disease states remains mostly a mystery. Scientists have not yet found a way to record the activity of more than a small number of neurons at once, non-invasively in living tissue.

Discussed in the March 2013 issue of the journal Science, the BAM research program is primarily technology-building and will develop three types of tools: those that can help simultaneously image or record the individual activity of neurons within a network; those that can control the activity of every neuron individually; and those that can store, manage, analyze, model and share large-scale imaging and physiology data [2].

Researchers suggest that these tools might include molecule-size wireless microcircuits that could be deployed, untethered, in living brains to monitor neuronal activity. DNA molecules could be synthesized to serve as a “ticker-tape” record.

The hope is that the BAM project will be an open, international collaboration of scientists, engineers and theoreticians throughout academia and industry. The plan is to start with small-brained invertebrates such as the worm, fly or leech, and then move up in brain complexity, ultimately working in humans. The authors write that within five years, it should be possible to monitor and control tens of thousands of neurons, and within 15 years, 1 million neurons — with “markedly reduced invasiveness”.

Although it is not yet clear how much federal money will actually be approved for the project, it won’t be cheap — at least $300 million a year, or $3 billion over a decade. However, during his 2013 State of the Union address, President Obama highlighted brain research as a leading candidate for government funding and alluded to the positive effect a project like BAM could have on the economy. He likened the BAM project to the Human Genome Project, which cost taxpayers $3.8 billion, but had a significant return on investment, returning $140 for every dollar invested.

Ray Suarez from PBS NewsHour recently interviewed Dr. Francis Collins, Director of the National Institutes of Health, which would coordinate much of the BAW project. You can watch the interview below.

The organizations slated to participate in the planning and funding of the BAM project include the Office of Science and Technology Policy, the National Institutes of Health, the Defense Advanced Research Projects Agency (DARPA), the National Science Foundation, and private foundations, such as the Howard Hughes Medical Institute.

References

1. Alivisatos et al. The brain activity map project and the challenge of functional connectomics. Neuron. 2012 Jun 21;74(6):970-4. doi: 10.1016/j.neuron.2012.06.006.
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2. Alivisatos et al. The Brain Activity Map. Science. 2013 Mar 7. [Epub ahead of print]
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As part of the U.S. Food and Drug Administration (FDA), the Center for Drug Evaluation and Research (CDER) promotes and protects the health of Americans by assuring that all prescription and over-the-counter drugs are safe and effective. The CDER evaluates all new over-the-counter and prescription drugs, including biological therapeutics and generic drugs, before they are sold.

The 39 novel approvals for 2012 encompass a number of new cancer therapies, including Roche’s Erivedge, the first FDA-approved drug for late-stage basal cell cancer, the most common form of skin cancer, Genentech’s Perjeta, approved for the 20% of breast cancer patients with HER2 positive cancers, and Medivation’s Xtandi, approved for castration-resistant prostate cancer, one of a new class of drugs known as androgen inhibitors, designed to interfere with the ability of testosterone to bind to prostate cancer cells. Testosterone is the male hormone that fuels prostate cancer cell growth. A detailed list of all new approved therapeutics is shown in the table below.

Positron Emission Tomography (PET) is an imaging technique that employs tracer compounds labelled with positron-emitting radionuclides as molecular probes. Once injected into a patient, the tracers are used to track biochemical and physiological processes in living cells. Two new PET tracers were approved in 2012: one for estimation of beta-amyloid neuritic plaque density in adult patients being evaluated for Alzheimer’s Disease and other causes of cognitive decline, and the second to help detect sites of prostate cancer.

Additional novel products approved in 2012 include treatments for cystic fibrosis, HIV, irritable bowel syndrome, vitreomacular adhesion, glaucoma, seizures and rheumatoid arthritis.

The 39 new drugs and biological products approved by the FDA for 2012 compares with 30 in 2011 and just 21 in 2010. At least 10 of the drugs had fast track status in 2012, which enabled them to be reviewed more quickly. Fast track is a process designed to facilitate the development, and expedite the review of drugs to treat serious diseases and fill an unmet medical need. The purpose of fast track status is to get important new drugs to the patient earlier.

The rise of targeted therapies was also a significant contributor to the FDA’s ability to reach decisions quickly and efficiently. Genomics technologies today are a drug development tool that radically streamlines drug targeting and enables much more efficient clinical development in the patients most likely to benefit from the drug.

In addition, two novel vaccines were also approved for use in 2012. Novartis’ Flucelvax is a seasonal influenza vaccine produced using cultured animal cells, the first alternative to the lengthy production of conventional flu vaccines in eggs. GSK’s MenHibrix is a combination vaccine for use in infants and toddlers aged 6 weeks to 18 months for prevention of invasive meningococcal disease.

CDER’s Novel Approvals In 2012

References

1. Are the 90s Back? Oncologists Drove FDA’s 2012 Novel Approval Count to 15-year High. Pharmaceutical Approvals Monthly. Elsevier Business Intelligence. 2013 Jan.

Green tea is rich in a group of antioxidant known as catechins. Antioxidants are important for neutralizing free radicals that we absorb form the environment and that can damage DNA, leading to tumor formation. Epigallocatechin-3-gallate (EGCG) is the most common catechin in tea leaves; it is found in green tea but not black tea, because the oxidation process used to make black tea destroys it.

The new study was based on a number of premises. First, there is epidemiological evidence that green tea consumption is inversely correlated with the incidence of Alzheimer’s disease, Parkinson’s disease, and dementia. Next, work done in animals suggests that EGCG protects against age-related cognitive decline. And last, it is known that new nerves can be generated in the hippocampus, even in adults. The hippocampus is a region of the brain important for consolidating short-term memories into long-term memories, and it also plays a role in spatial navigation. The generation of new neurons in the hippocampus, a process called hippocampal neurogenesis, declines with age, and this decline is associated with neurodegenerative diseases and the memory problems and disorientation that accompany them. Thus, the researchers wanted to see if EGCG might alleviate neurodegeneration by promoting hippocampal neurogenesis in adults, and if so, how.

They applied EGCG to murine neural progenitor cells growing in dishes and found that EGCG enhanced the proliferation of these cells. When they isolated hippocampal neurons from adult mice that had been injected with ECGC, they found that those cells, too, grew more than cells from mice who received a control injection of saline. Moreover, the mice who received an injection of ECGC exhibited improved spatial learning and memory; treated mice found a hidden platform more quickly than control mice.

When they looked for the molecular modulator of ECGC’s ability to stimulate neuronal growth in the hippocampus their attention fell upon sonic hedgehog (SHH), a protein vital in both the development of the brain during embryogenesis as well as maintenance of neural progenitor cells in the adult brain. And yes, it is named for the video game character. It turns out that ECGC increases the amount of sonic hedgehog, as well as some of its interaction partners, in hippocampal neural progenitor cells. An inhibitor of sonic hedgehog signaling partially blocked ECGC’s ability to promote neuronal growth, strongly suggesting that ECGC uses sonic hedgehog to exert this activity.

The authors note that ECGC is being considered for use as a preventative and therapeutic agent in the treatment of neurodegenerative disease, and their findings that ECGC helps promote adult hippocampal neurogenesis by signaling through sonic hedgehog certainly supports this course of action. Although much of the evidence for green tea’s potency comes from laboratory studies such as this one, rather than human clinical trials, they also suggest that drinking green tea can have positive effects on cognition. Just don’t put milk in it; the proteins in milk, be it from a cow or a soybean, bind to ECGC and reduces the body’s ability to make use of it [2].

References

1. Wang et al. Green tea epigallocatechin-3-gallate (EGCG) promotes neural progenitor cell proliferation and sonic hedgehog pathway activation during adult hippocampal neurogenesis. Mol Nutr Food Res. 2012 Aug;56(8):1292-303. doi: 10.1002/mnfr.201200035. Epub 2012 Jun 13.
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2. Egert et al. Simultaneous ingestion of dietary proteins reduces the bioavailability of galloylated catechins from green tea in humans. Eur J Nutr. 2012 Feb 25. [Epub ahead of print]
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Using real time imaging, scientists examined mitochondria in live neurons from three different mouse models of Alzheimer’s disease. Each of the mouse models had a different gene mutation shown to cause familial, or early-onset, Alzheimer’s disease. To evaluate the the impact of a given mutation, mitochondrial motility, distribution, ultrastructure and function in neurons and brain tissue was examined early in mouse development until the age where mice began to display memory loss and amyloid deposits formed.

Researchers used a mitochondria-specific dye and monitored axonal trafficking (i.e. motion along axons or nerve fibers). The investigators found that mitochondrial axonal trafficking is inhibited in embryonic neurons afflicted with Alzheimer’s disease, well before mice showed any memory loss or amyloid plaque formation.
Indeed, inhibition of axonal trafficking was found to be a general defect that occurred in all three mouse models of Alzheimer’s disease and was not specific for mitochondria. Nevertheless, neurons with inhibited mitochondrial trafficking were found to be more susceptible to excitotoxic cell death, a pathological process wherein nerve cells are killed by excessive neurotransmitter stimulation.

In the brains of all three mouse models of Alzheimer’s disease, mitochondria tended to lose their integrity and subsequently stopped functioning. Importantly, dysfunctional mitochondria were detected at the synapses of neurons involved in maintaining memory, suggesting a direct linkage with Alzheimer’s disease.

The scientists also applied a method called metabolomics, which measures the chemical fingerprints of specific metabolic pathways in the cell such as sugars, lipids, nucleotides, amino acids and fatty acids. The approach takes a snapshot of what is happening in the body at a given time and at a hight level of detail, and provides insight into the cellular processes that underlie a disease. For this study, the metabolomic profiles showed changes in metabolites related to mitochondrial function and cellular energy metabolism, which further confirmed that altered mitochondrial energetics is fundamental to the disease process.

The researchers identified a panel of metabolomic biomarkers. According to Eugenia Trushina, Ph.D., Mayo Clinic pharmacologist and senior investigator on the study [2]:

We are not looking at the consequences of Alzheimer’s disease, but at very early events and molecular mechanisms that lead to the disease. We expect to validate metabolomic changes in humans with Alzheimer’s disease and to use these biomarkers to diagnose the disease before symptoms appear — which is the ideal time to start treatment.

The researchers conclude by stating that Alzheimer’s disease can be viewed as a mitochondrial movement disorder with evolving energetic deficit represented by the panel of metabolomic biomarkers and that mitochondrial dysfunction is an underlying event in Alzheimer’s disease progression.

References

1. Trushina et al. Defects in mitochondrial dynamics and metabolomic signatures of evolving energetic stress in mouse models of familial Alzheimer’s disease. PLoS One. 2012;7(2):e32737. Epub 2012 Feb 29.
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2. Mitochondrial Dysfunction Present Early in Alzheimer’s, Before Memory Loss. Mayo Clinic News. 2012 Feb 29.

Image credit: Blueberry, strawberry, raspberry and blackberry via Shutterstock

Many of these changes appear to be due to oxidative processes, which are chemical changes that occur as a result of exposure to radiation, toxins, environmental factors, and naturally occurring chemicals. Oxidative processes are a natural part of aging, and contribute to many of the effects of aging (both in and outside the brain), including cancer and other diseases. Changes in brain function (and other body functions) due to oxidative processes become more pronounced with increasing age because oxidative changes accumulate over time, and because advancing age is associated with a decline in the body’s antioxidant systems [3].

Researchers have long known that consumption of antioxidant chemical-containing foods is beneficial in staving off the oxidation-related effects of aging. While many fruits and vegetables are good sources of antioxidant chemicals, berries are a particularly rich source of a class of antioxidant chemicals called anthocyanins [4]. A new review of studies suggests that mounting evidence supports consumption of berries to help maintain brain function with age [5].

The review authors note that there is in vitro evidence to support berry consumption for brain health. Examples include studies that show constituents of berries affect neuronal signaling and neurotransmitter production [6-8]. As for in vivo evidence, aging rats fed berries on a routine basis showed improved memory [9] and improved recognition of a new object [10]. The anti-inflammatory properties of berries have been replicated in vivo [11], and berries have been demonstrated to reduce neuronal atrophy in aging rats [12]. Clinical evidence in humans is also beginning to accumulate, though research on the effects of berries on the aging human brain is not yet conclusive.

Nevertheless, given that berries are a healthy component of diet aside from any potential anti-aging properties they might possess (they’re high in vitamin C and certain minerals, including selenium), a risk-to-benefit analysis supports incorporating berries into the diet on a regular basis.

References

1. Verhaeghen et al. Aging, executive control, and attention: a review of meta-analyses. Neurosci Biobehav Rev. 2002 Nov;26(7):849-57.
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2. Seidler et al. Motor control and aging: links to age-related brain structural, functional, and biochemical effects. Neurosci Biobehav Rev. 2010 Apr;34(5):721-33. Epub 2009 Oct 20.
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3. Sohal et al. Oxidative stress, caloric restriction, and aging. Science. 1996 Jul 5;273(5271):59-63.
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4. Winkel-Shirley, B. Biosynthesis of flavonoids and effects of stress. Curr Opin Plant Biol. 2002 Jun;5(3):218-23.
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5. Miller et al. Berry Fruit Enhances Beneficial Signaling in the Brain. J Agric Food Chem. 2012 Feb 3. [Epub ahead of print].
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6. Dreiseitel et al. Berry anthocyanins and their aglycons inhibit monoamine oxidases A and B. Pharmacol Res. 2009 May;59(5):306-11. Epub 2009 Feb 5.
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7. Joseph et al. The m3 muscarinic receptor i3 domain confers oxidative stress protection on calcium regulation in transfected cos-7 cells. Aging Cell. 2004 Oct;3(5):263-71.
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8. Kim et al. Mulberry fruit protects dopaminergic neurons in toxin-induced Parkinson’s disease models. Br J Nutr. 2010 Jul;104(1):8-16. Epub 2010 Feb 26.
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9. Shukitt-Hale et al. The effects of grape juice on cognitive and motor deficits in aging. Nutrition. 2006 Mar;22(3):295-302. Epub 2006 Jan 18.
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10. Goyarzu et al. Blueberry supplemented diet: effects on object recognition memory and nuclear factor-kB levels in aged rats. Nutr Neurosci. 2004 Apr;7(2):75-83.
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11. Ueda et al. Glutamate excess and free radical formation during and following kainic acid-induced status epilepticus. Exp Brain Res. 2002 Nov;147(2):219-26. Epub 2002 Sep 25.
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12. Shih et al. Antioxidant and cognitive promotion effects of anthocyanin-rich mulberry (Morus atropurpurea L.) on senescence-accelerated mice and prevention of Alzheimer’s disease. J Nutr Biochem. 2010 Jul;21(7):598-605. Epub 2009 May 14.
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Using a combination of lasers and genetic engineering, Boyden’s lab implants brains with optical fibers that allow them to activate special proteins in specific neurons and see their connections. In addition to helping create detailed maps of brain circuitry, the engineering of these cells has been used to cure blindness in mice, and could point the way to cures for Parkinson’s disease or Alzheimer’s disease. On the horizon: ways of connecting to the brain via prosthetics.

By inserting genes for light-sensitive proteins into brain cells, neurons can be selectively activated or de-activated with fiber-optic implants. Check out Boyden’s demonstration at TED2011 below.

Dr. Segal’s lab recently published a study investigating the cellular machinery involved in long-term memory storage, focusing specifically on dendritic spines: small protrusions from the cell body, less than a mm in length, onto which synapses are made [1].

Neurons, or nerve cells, are the primary cell type in an animal’s nervous system. Their most distinguishing feature is the ability to conduct signals along their length. These signals can be transmitted via electrical messengers, like the voltage changes accomplished by the movement of charged particles including sodium, potassium, calcium and chloride in and out of the cells; or via chemical messengers, neurotransmitters such as dopamine and serotonin.

Dendrites are long thin structures that arise from the cell body branch multiple times. The cell body of a neuron frequently gives rise to multiple dendrites; these function to receive electrical signals from neighboring neurons and conduct them to the cell body from which they originate.

Dendrite spines are protrusions that extend out of the dendrite. Each spine can receive signals, and the more signaling that occurs through a particular spine, the more it grows. This growth is thought to be important in learning and memory formation. The dendrites of a single neuron can contain hundreds to thousands of spines, thus increasing the number of contacts between neurons.

The great variety of dendritic spine shapes, sizes, and density of distribution on the parent dendrites of a single neuron, as well as the apparent persistence of spines throughout the life of each neuron, suggest that these spines are involved in memory formation and storage. While this view prevailed throughout the 20th century, supporting evidence for it is rather scarce because the small size of the spine prevents systematic electrophysiological analysis.

It has been known for some time that a particular enzyme known as protein kinase C, zeta form (PKMz or PRKCZ) is important for long-term memory storage. Indeed, last year during Brain Awareness Week, we reported that memory enhancement had been achieved in rats; one of the studies discussed utilized PRKCZ to enhance the rats’ long-term memories of a conditioned taste aversion.  What hasn’t been understood, however, is how PRKCZ — also called PKMz — maintains or enhances memory. Dr. Segal and the members of his lab thus put extra copies of PKMz into rat neurons growing in tissue culture dishes and examined what happened to their dendritic spines. Using time lapse photography of these living cultured neurons in a confocal laser scanning microscope, they showed that the extra PKMz did not change the number of spines or the number of branches each spine had, which indicates the number of synapses it can form. However, it did reduce the length of the spines, making them stubbier and more mushroom-like; this is a hallmark of more mature spines. These spines are more stable than longer and thinner spines, which represent newly formed synapses and can appear and disappear within days.

The researchers concluded that PKMz accumulates in pre-existing dendritic spines and helps them mature, and that it uses this mechanism to play its previously known but not yet elucidated role in maintaining or enhancing long-term memory. In future studies, Dr. Segal and his team hope to begin to uncover the cellular basis of the neuroplasticity exhibited by developing brains.

References

1. Ron et al. Overexpression of PKMz Alters Morphology and Function of Dendritic Spines in Cultured Cortical Neurons. Cereb Cortex. 2011 Nov 28. [Epub ahead of print]
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Image credit: Neurons network in human brain via Shutterstock

A hallmark of Alzheimer’s Disease is the accumulation of ‘neurofibrillary tangles,’ aggregated clumps of a mutated form of microtubule associated protein tau (MAPT).

In the earliest stages of Alzheimer’s Disease, these tangles accumulate primarily in the entorhinal cortex (EC), a region of the brain involved in memory formation and consolidation. As the disease progresses, these tau aggregates can be seen in the hippocampus and other areas of the brain. But it is not clear whether the pathology that starts in the entorhinal cortex travels to these other brain regions, or if it arises there independently.

To date, mouse models of Alzheimer’s have been made that have high levels of tau aggregates all over the brain. These have provided valuable insights into the disease, but could not be used to analyze its molecular progression over time or space. Scientists in Karen Duff’s lab at the Taub Institute for Alzheimer’s Disease Research, Columbia University, New York, just made new mice that express the pathological version of human tau protein only in the entorhinal cortex. They then compared the distribution of tau aggregates in young mice and old mice.

As the mice aged, the scientists found that the tau aggregates spread from the entorhinal cortex to regions that are connected to it through one or more synapses, like the hippocampus and neocortex. The hippocampus is important in cementing short term memories into long term memories and is also involved in spatial navigation, and the neocortex plays a role in higher level cognitive functions like conscious thought and language. Although the mechanism by which these tau aggregates affect neurodegeneration is not quite known, their accumulation has definitely been correlated with more severe pathology and ultimately neuronal cell death.

This new mouse model shows that Alzheimer’s Disease progresses through what the authors call an “anatomical cascade,” rather than developing multiple times in independent events spread throughout the brain. The earliest stages of the disease, when the tau tangles are restricted to the entorhinal cortex and connected areas, are not associated with any mental decline. The authors thus hope that the location of these ‘neurofibrillary tangles’ can now be used as a temporal biomarker, and that strategies might soon be developed to halt their spread.

References

1. Liu et al. Trans-Synaptic Spread of Tau Pathology In Vivo. PLoS One. 2012;7(2):e31302. Epub 2012 Feb 1.
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• Recent Advances in Biomarker Discovery for Parkinson’s disease, a Satellite Symposium at the Society for Neuroscience Annual Meeting

  A satellite symposium, Recent Advances in Biomarker Discovery for Parkinson’s Disease, is being sponsored by Covance on November 13th, 2011 at the Society for Neuroscience Annual Meeting in Washington, D.C.

• NYAS Symposium: Biomarkers and Brain Imaging of Presymptomatic Alzheimer’s Disease

  The New York Academy of Sciences (NYAS) will be holding an afternoon event in January 2012 that focuses on biomarkers and brain imaging of presymptomatic Alzheimer’s disease.

• NIH to Support Clinical Trial Implementation or Biomarker Clinical Evaluation Studies

  Earlier this month, the National Institutes of Health announced that the National Institute of Dental and Craniofacial Research (NIDCR) Institute will support mission-relevant investigator-initiated Phase I, II, III or IV clinical trial cooperative agreement applications or biomarker evaluation studies that require prospective collection of clinical outcomes and clinical specimens.

• NIH to Fund Studies that Adapt Adult Biomarkers to Children

  The National Institutes of Health announced Thursday that the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) will support studies that propose adapting adult biomarkers to children.

• CLC bio to Develop Bioinformatics Tools for Prostate Cancer Biomarker Project

  CLC bio is participating in a $4 million Danish collaboration focused on the identification and validation of biomarkers of prostate cancer risk and aggressiveness.

Walter Koroshetz, M.D., deputy director of NIH’s National Institute of Neurological Disorders and Stroke (NINDS), said:

There are many traumatic brain injury studies whose value to scientific research and clinical care could be greatly enhanced by transforming the data into a common, easily available format.

In the United States, about 1.7 million people sustain traumatic brain injuries each year from common causes such as falls and auto accidents. In addition, American Service members serving in Iraq, Afghanistan and other parts of the world face unique risks of traumatic brain injury from routine military operations, enemy fire and improvised explosive devices. According to the DoD, in the past 12 years, more than 200,000 service members deployed worldwide have been diagnosed with traumatic brain injury, adding to the urgent need for preventive methods and treatments. Total costs of traumatic brain injury in the U.S., including medical care, lost wages and other expenses, exceed $60 billion.

Colonel Dallas Hack, director of the U.S. Army Combat Casualty Research Program and joint chairperson for the Defense Health Program, said:

Despite the great burden of neurotrauma incidence, developing objective diagnostics and treatments has proven especially challenging for the medical community. Only by combining efforts through initiatives such as the FITBIR database can we hope to make major progress in this field.

Despite improved surgeries and rehabilitation techniques for people with brain injuries, treatments remain limited. Cases of traumatic brain injury are highly variable, involving different causes, locations within the brain and different kinds of damage to brain tissue. Such variability makes it difficult for clinicians to treat patients, predict long-term outcomes and investigate new therapies. Also, studies often report different kinds of data on patients, obtained through various tests and measures, further impeding comparison of data across studies. The FITBIR database will address these challenges by collecting uniform and high-quality data on traumatic brain injury, including brain imaging scans and neurological test results. The data will be obtained with informed consent and stripped of any patient-identifying information.

Matthew McAuliffe, Ph.D., co-director of the FITBIR database and a member of NIH’s Center for Information Technology (CIT), said:

Uniform data makes it much easier to compare intervention results across a broad range of studies, providing innovative and unique insights that are not possible from a single study. This is part of a larger effort by the government to make taxpayer-funded research more broadly available and usable.

The database is expected to aid in the development of:

• A system to classify different types of traumatic brain injury
• More targeted studies to determine which treatments are effective and for whom and under what conditions (comparative effectiveness research)
• Enhanced diagnostic criteria for concussions and milder injuries
• Predictive markers to identify those at risk of developing conditions that have been linked to traumatic brain injury, such as Alzheimer’s disease
• Clearer understanding of the effects of age, sex, and other medical conditions on injury and recovery
• Improved evidence-based guidelines for patient care, from the time of injury through rehabilitation

NIH CIT was chosen to build the database because of its experience and success in developing the National Database on Autism Research. Reusing the database structure is expected to save 35-50 percent of the project costs and significantly reduce the time to achieve meaningful results.

The database builds upon a larger effort to create common data elements for the study of traumatic brain injury — which are essentially definitions and guidelines about the kinds of data that should be collected, and how to collect these data in clinical studies. The Common Data Elements project emerged from a collaborative interagency effort involving over 50 American and European universities and several federal agencies, including the National Institute of Neurological Disorders and Stroke (NINDS), Defense and Veterans Brain Injury Center (DVBIC), Defense Centers of Excellence for Psychological Health and Traumatic Brain Injury (DCoE), Department of Veterans Affairs and the National Institute on Disability and Rehabilitation Research within the Department of Education.

The Defense Health Program, through agreement with the U.S. Army Medical Research and Materiel Command (USAMRMC) is the lead DoD component funding the FITBIR database. The Division of Computational Bioscience within NIH CIT is building the database, and will provide ongoing system administration and hosting services once the database is complete in about two years.

The U.S. Army Medical Research and Materiel Command (USAMRMC) and NINDS will provide programmatic support and foster collaborative research to populate the database. Researchers will be given detailed information about the FITBIR database, and encouraged to participate at the time they submit proposals for new studies.

Source: NIH News