Neuroscience

Articles and news from the latest research reports.

Posts tagged science

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Veterans with mild traumatic brain injury have brain abnormalities Mild traumatic brain injury (TBI), including concussion, is one of the most common types of neurological disorder, affecting approximately 1.3 million Americans annually. It has received more attention recently because of its frequency and impact among two groups of patients: professional athletes, especially football players; and soldiers returning from mid-east conflicts with blast-related TBI. An estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan have experienced TBI. A recent study by psychiatrists from the Iowa City VA Medical Center and University of Iowa Health Care finds that soldiers returning from Iraq and Afghanistan with mild TBI have measurable abnormalities in the white matter of their brains when compared to returning veterans who have not experienced TBI. These abnormalities appear to be related to the severity of the injury and are related to cognitive deficits. The findings were published online in December in the American Journal of Psychiatry.

Veterans with mild traumatic brain injury have brain abnormalities

Mild traumatic brain injury (TBI), including concussion, is one of the most common types of neurological disorder, affecting approximately 1.3 million Americans annually.

It has received more attention recently because of its frequency and impact among two groups of patients: professional athletes, especially football players; and soldiers returning from mid-east conflicts with blast-related TBI. An estimated 10 to 20 percent of the more than 2 million U.S. soldiers deployed in Iraq or Afghanistan have experienced TBI.

A recent study by psychiatrists from the Iowa City VA Medical Center and University of Iowa Health Care finds that soldiers returning from Iraq and Afghanistan with mild TBI have measurable abnormalities in the white matter of their brains when compared to returning veterans who have not experienced TBI. These abnormalities appear to be related to the severity of the injury and are related to cognitive deficits. The findings were published online in December in the American Journal of Psychiatry.

Filed under brain TBI white matter diffusion tensor imaging cognitive deficits neuroscience science

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Hopkins Researchers Uncover Key to Antidepressant Response Through a series of investigations in mice and humans, Johns Hopkins researchers have identified a protein that appears to be the target of both antidepressant drugs and electroconvulsive therapy. Results of their experiments explain how these therapies likely work to relieve depression by stimulating stem cells in the brain to grow and mature. In addition, the researchers say, these experiments raise the possibility of predicting individual people’s response to depression therapy, and fine-tuning treatment accordingly. Reports on separate aspects of the research were published in December on the Molecular Psychiatry website, and will also appear in the Feb. 7 issue of Cell Stem Cell.

Hopkins Researchers Uncover Key to Antidepressant Response

Through a series of investigations in mice and humans, Johns Hopkins researchers have identified a protein that appears to be the target of both antidepressant drugs and electroconvulsive therapy. Results of their experiments explain how these therapies likely work to relieve depression by stimulating stem cells in the brain to grow and mature. In addition, the researchers say, these experiments raise the possibility of predicting individual people’s response to depression therapy, and fine-tuning treatment accordingly. Reports on separate aspects of the research were published in December on the Molecular Psychiatry website, and will also appear in the Feb. 7 issue of Cell Stem Cell.

Filed under depression antidepressant drugs electroconvulsive therapy stem cells neuroscience science

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In the brain, broken down ‘motors’ cause anxiety When motors break down, getting where you want to go becomes a struggle. Problems arise in much the same way for critical brain receptors when the molecular motors they depend on fail to operate. Now, researchers reporting in Cell Reports, a Cell Press publication, on February 7, have shown these broken motors induce stress and anxiety in mice. The discovery may point the way to new kinds of drugs to treat anxiety and other disorders. The study in mice focuses on one motor in particular, known as KIF13A, which, according to the new evidence, is responsible for ferrying serotonin receptors. Without proper transportation, those receptors fail to reach the surface of neurons and, as a result, animals show signs of heightened anxiety. In addition to their implications for understanding anxiety, the findings also suggest that defective molecular motors may be a more common and underappreciated cause of disease. "Most proteins are transported in vesicles or as protein complexes by molecular motors," said Nobutaka Hirokawa of the University of Tokyo. "As shown in this study, defective motors could cause many diseases." Scientists know that serotonin and serotonin receptors are involved in anxiety, aggression, and mood. But not much is known about how those players get around within cells. When Hirokawa’s team discovered KIF13A at high levels in the brain, they wondered what it did. The researchers discovered that mice lacking KIF13A show greater anxiety in both open-field and maze tests and suggest that this anxious behavior may stem from an underlying loss of serotonin receptor transport, which leads to a lower level of expression of those receptors in critical parts of the brain. "Collectively, our results suggest a role for this molecular motor in anxiety control," the researchers wrote. Hirokawa says the search should now be on for anti-anxiety drug candidates aimed at restoring the brain’s serotonin receptor transport service.

In the brain, broken down ‘motors’ cause anxiety

When motors break down, getting where you want to go becomes a struggle. Problems arise in much the same way for critical brain receptors when the molecular motors they depend on fail to operate. Now, researchers reporting in Cell Reports, a Cell Press publication, on February 7, have shown these broken motors induce stress and anxiety in mice. The discovery may point the way to new kinds of drugs to treat anxiety and other disorders.

The study in mice focuses on one motor in particular, known as KIF13A, which, according to the new evidence, is responsible for ferrying serotonin receptors. Without proper transportation, those receptors fail to reach the surface of neurons and, as a result, animals show signs of heightened anxiety.

In addition to their implications for understanding anxiety, the findings also suggest that defective molecular motors may be a more common and underappreciated cause of disease.

"Most proteins are transported in vesicles or as protein complexes by molecular motors," said Nobutaka Hirokawa of the University of Tokyo. "As shown in this study, defective motors could cause many diseases."

Scientists know that serotonin and serotonin receptors are involved in anxiety, aggression, and mood. But not much is known about how those players get around within cells. When Hirokawa’s team discovered KIF13A at high levels in the brain, they wondered what it did.

The researchers discovered that mice lacking KIF13A show greater anxiety in both open-field and maze tests and suggest that this anxious behavior may stem from an underlying loss of serotonin receptor transport, which leads to a lower level of expression of those receptors in critical parts of the brain.

"Collectively, our results suggest a role for this molecular motor in anxiety control," the researchers wrote. Hirokawa says the search should now be on for anti-anxiety drug candidates aimed at restoring the brain’s serotonin receptor transport service.

Filed under anxiety brain serotonin receptors neurons proteins neuroscience medicine science

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Subcortical Damage Is ‘Primary Cause’ of Neurological Deficits after ‘Awake Craniotomy’

Injury to the subcortical structures of the inner brain is a major contributor to worsening neurological abnormalities after “awake craniotomy” for brain tumors, reports a study in the February issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

During a procedure intended to protect critical functional areas in the outer brain (cortex), damage to subcortical areas—which may be detectable on MRI scans—is a major risk factor for persistent neurological deficits. “Our ability to identify and preserve cortical areas of function can still result in significant neurological decline postoperatively as a result of subcortical injury,” write Dr. Victoria T. Trinh and colleagues of The University of Texas MD Anderson Cancer Center, Houston.

Risk Factors for Neurological Deficits after Awake Craniotomy

The researchers analyzed factors associated with worsening neurological function after awake craniotomy for brain tumor surgery. In awake craniotomy, the patient is sedated but conscious so as to be able to communicate with the surgeon during the operation.

The patient is asked to perform visual and verbal tasks while specific areas of the cortex are stimulated, generating a functional map of the brain surface. This helps the surgeon navigate safely to the tumor without damaging the “eloquent cortex”—critical areas of the brain involved in language or movement.

The study included 241 patients who underwent awake craniotomy with functional brain mapping from 2005 through 2010. Of these, 40 patients developed new neurological abnormalities. Dr. Trinh and colleagues examined potential predictive factors—including changes on a type of MRI scan called diffusion-weighted imaging (DWI).

Of the 40 cases with new neurological deficits, 36 developed while the surgeon was operating in the subcortical areas of the brain. These are the inner structures of the brain, located beneath the outer, folded brain cortex. Just one abnormality developed while the surgeon was operating in the cortex only.

MRI Changes May Reflect Subcortical Damage

Neurological abnormalities developing while the surgeon was operating in the subcortex were likely to remain after surgery, and to persist at three months’ follow-up evaluation. Dr. Trinh and coauthors write, “Patients with intraoperative deficits during subcortical dissection were over six times more likely to have persistently worsened neurological function at three-month follow-up.”

In these patients, MRI scans showing more severe changes in the DWI pattern in the subcortex also predicted lasting neurological abnormalities. Of patients who had neurological deficits immediately after surgery and significant DWI changes, 69 percent had persistent deficits three months after surgery.

Patients who had “positive” cortical mapping—that is, in whom eloquent cortex was located during functional mapping—were somewhat more likely to have neurological abnormalities immediately after surgery. However, the risk of lasting abnormalities was not significantly higher compared to patients with negative cortical mapping.

Awake craniotomy with brain stimulation produces a “real-time functional map” of the brain surface that is invaluable to the neurosurgeon in deciding how best to approach the tumor. The new results suggest that, even when the eloquent cortex is not located on cortical mapping, subcortical areas near the tumor can still be injured during surgery. “Subcortical injury is the primary cause of neurological deficits following awake craniotomy procedures,” Dr. Trinh and colleagues write.

The researchers add, “Preserving subcortical areas during tumor resections may reduce the severity of both immediate and late neurological sequelae.” Based on their findings, they believe subcortical mapping techniques may play an important role in avoiding complications after awake craniotomy.

(Source: lww.com)

Filed under brain brain tumors craniotomy cortex MRI neuroscience science

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How chronic pain disrupts short term memory A group of Portuguese researchers from IBMC and FMUP at the University of Porto has found the reason why patients with chronic pain often suffer from impaired short –term memory. The study, to be published in the Journal of Neuroscience, shows how persistent pain disrupts the flow of information between two brain regions crucial to retain temporary memories. Chronic pain suffers often complain of short term memory’s problems. The neural mechanisms why this occurs are however not understood. Recent studies in animals showed that pain can disturb several cognitive processes as well as change the brain pathways for how we think and feel. Of the many cognitive disturbances observed the most important include problems in spatial memory, recognition memory, attention and even emotional and non-emotional decisions. In the new article the team of researchers from the University of Porto led by Vasco Gallardo describes in a rat model of neuropathic pain how a neuronal circuit crucial for the processing of short-term memory is affected by pain. The circuit, established between the prefrontal cortex and the hippocampus, is essential for encoding and retaining temporary memories on spatial information. The researchers used multi-electrodes implanted in the brain to record neuronal activity during a behaviour dependent of spatial memory - the animals were trained in a maze where they had to choose between two alternative paths and then asked to recall their chosen path. The results show that after a painful injury there is a significant reduction in the amount of information that passes through the circuit. This could mean a loss of ability to process information on spatial localization memory, or that those regions critical to memory are now “overwhelmed” by the painful stimuli disrupting the flow of information for memory. According to Vasco Gallardo, the team ” has already demonstrated that peripheral nerve injury induces an instability in the spatial coding capacity of hippocampus neurons “, where is seen “a clear reduction in their capacity to encode information on the location of the animal.” So to the author “this new work contributes to the demonstration that chronic pain induces alterations in the function of brain circuits that are not directly connected to tactile or painful processes”. So as a result of chronic pain it is seen that “are also affected neuronal circuits linked to the processing of memories and emotions, what might mean a need for larger and more integrative strategies in the treatment of painful pathologies”, says the researcher.

How chronic pain disrupts short term memory

A group of Portuguese researchers from IBMC and FMUP at the University of Porto has found the reason why patients with chronic pain often suffer from impaired short –term memory. The study, to be published in the Journal of Neuroscience, shows how persistent pain disrupts the flow of information between two brain regions crucial to retain temporary memories.

Chronic pain suffers often complain of short term memory’s problems. The neural mechanisms why this occurs are however not understood. Recent studies in animals showed that pain can disturb several cognitive processes as well as change the brain pathways for how we think and feel. Of the many cognitive disturbances observed the most important include problems in spatial memory, recognition memory, attention and even emotional and non-emotional decisions.

In the new article the team of researchers from the University of Porto led by Vasco Gallardo describes in a rat model of neuropathic pain how a neuronal circuit crucial for the processing of short-term memory is affected by pain. The circuit, established between the prefrontal cortex and the hippocampus, is essential for encoding and retaining temporary memories on spatial information. The researchers used multi-electrodes implanted in the brain to record neuronal activity during a behaviour dependent of spatial memory - the animals were trained in a maze where they had to choose between two alternative paths and then asked to recall their chosen path.

The results show that after a painful injury there is a significant reduction in the amount of information that passes through the circuit. This could mean a loss of ability to process information on spatial localization memory, or that those regions critical to memory are now “overwhelmed” by the painful stimuli disrupting the flow of information for memory.

According to Vasco Gallardo, the team ” has already demonstrated that peripheral nerve injury induces an instability in the spatial coding capacity of hippocampus neurons “, where is seen “a clear reduction in their capacity to encode information on the location of the animal.”

So to the author “this new work contributes to the demonstration that chronic pain induces alterations in the function of brain circuits that are not directly connected to tactile or painful processes”. So as a result of chronic pain it is seen that “are also affected neuronal circuits linked to the processing of memories and emotions, what might mean a need for larger and more integrative strategies in the treatment of painful pathologies”, says the researcher.

Filed under chronic pain STM recognition memory neuronal activity hippocampus neuroscience science

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Translation error tracked in the brain of dementia patients In certain dementias silent areas of the genetic code are translated into highly unusual proteins by mistake. An international team of scientists including researchers from the German Center for Neurodegenerative Diseases (DZNE) in Munich and the Ludwig-Maximilians-Universität (LMU) present this finding in the online edition of “Science”. The proteins that have now been identified shouldn’t actually exist. Nevertheless, they build the core of cellular aggregates whose identity has been enigmatic until now. These aggregates are typically associated with hereditary neurodegenerative diseases including variants of frontotemporal dementia (FTD), also known as frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). They are likely to be damaging and might be a target for therapy. FTD and ALS are part of a group of neurodegenerative diseases that show a broad and overlapping variety of symptoms: Patients often suffer from dementia, personality changes and may also be affected by language abnormalities and movement disorders. The problems often arise before the age of 65 without a clear cause. However, about 30 percent of cases are linked to a genetic cause. In Europe approximately 10 percent of patients show a common genetic feature: In their DNA (the carrier of the genetic code) a particular short sequence appears in numerous copies one after another. Furthermore, proteins of unknown identity accumulate inside the brain of these patients. As it turns out both findings are directly related – that is what the team of researchers including molecular biologists Dieter Edbauer and Christian Haass has now been able to show. “We have found that the proteins are linked to a genetic peculiarity which many patients have in common. At a certain location inside the gene C9orf72 there are several hundred repeats of the sequence GGGGCC, while healthy people display less than 20 such copies,” explains Prof. Edbauer, who researches at the DZNE and the LMU. “But it is surprising that these proteins are actually made, because these repeats fall into a region of the DNA that should not be translated into proteins.” An area of DNA assumed to be silent The DNA holds the blueprints for building proteins. In general, the beginning of such a blueprint is indicated by a certain molecular start signal, but the usual signal is missing in this case. The region of DNA comprising the numerous repeats should therefore not be translated into proteins. It seems that the process of protein synthesis is initiated in a non-textbook way. “Although quite rare there are two known alternatives to the common mechanism. Which procedure applies here, we don’t know yet,” says Prof. Haass, Site Speaker of the DZNE in Munich and chair of Metabolic Biochemistry at LMU. Nevertheless, in cell culture experiments the researchers were able to show that long repeats of the sequence GGGGCC may in fact lead to the production of proteins, even though the usual start signal is missing. Furthermore, they identified the same proteins in the particles that typically accumulate in the brain of patients. The scientist could also identify their composition: They turned out to be dipeptid-repeat proteins, which comprise a very large number of identical building blocks. “These are very extraordinary proteins that usually don’t show-up in the organism,” Edbauer notes. “As far as we know, they are completely useless and scarcely soluble. Therefore, they tend to aggregate and seem to damage the nerve cells. We haven’t formally proven toxicity, but there is ample evidence.” Because of their peculiarity these proteins might be an interesting target for new therapies. “As the mechanism of their production is so unusual, we may find ways to inhibit their synthesis without interfering with the formation of other proteins. One could also try to block their aggregation and accelerate their decomposition.” The scientists have applied for a patent and are pursuing a major goal. “At the DZNE in Munich it is our dream to develop a therapy against these devastating diseases,“ Haass and Edbauer conclude.

Translation error tracked in the brain of dementia patients

In certain dementias silent areas of the genetic code are translated into highly unusual proteins by mistake. An international team of scientists including researchers from the German Center for Neurodegenerative Diseases (DZNE) in Munich and the Ludwig-Maximilians-Universität (LMU) present this finding in the online edition of “Science”. The proteins that have now been identified shouldn’t actually exist. Nevertheless, they build the core of cellular aggregates whose identity has been enigmatic until now. These aggregates are typically associated with hereditary neurodegenerative diseases including variants of frontotemporal dementia (FTD), also known as frontotemporal lobar degeneration (FTLD), and amyotrophic lateral sclerosis (ALS). They are likely to be damaging and might be a target for therapy.

FTD and ALS are part of a group of neurodegenerative diseases that show a broad and overlapping variety of symptoms: Patients often suffer from dementia, personality changes and may also be affected by language abnormalities and movement disorders. The problems often arise before the age of 65 without a clear cause. However, about 30 percent of cases are linked to a genetic cause. In Europe approximately 10 percent of patients show a common genetic feature: In their DNA (the carrier of the genetic code) a particular short sequence appears in numerous copies one after another. Furthermore, proteins of unknown identity accumulate inside the brain of these patients. As it turns out both findings are directly related – that is what the team of researchers including molecular biologists Dieter Edbauer and Christian Haass has now been able to show.

“We have found that the proteins are linked to a genetic peculiarity which many patients have in common. At a certain location inside the gene C9orf72 there are several hundred repeats of the sequence GGGGCC, while healthy people display less than 20 such copies,” explains Prof. Edbauer, who researches at the DZNE and the LMU. “But it is surprising that these proteins are actually made, because these repeats fall into a region of the DNA that should not be translated into proteins.”

An area of DNA assumed to be silent

The DNA holds the blueprints for building proteins. In general, the beginning of such a blueprint is indicated by a certain molecular start signal, but the usual signal is missing in this case. The region of DNA comprising the numerous repeats should therefore not be translated into proteins. It seems that the process of protein synthesis is initiated in a non-textbook way. “Although quite rare there are two known alternatives to the common mechanism. Which procedure applies here, we don’t know yet,” says Prof. Haass, Site Speaker of the DZNE in Munich and chair of Metabolic Biochemistry at LMU.

Nevertheless, in cell culture experiments the researchers were able to show that long repeats of the sequence GGGGCC may in fact lead to the production of proteins, even though the usual start signal is missing. Furthermore, they identified the same proteins in the particles that typically accumulate in the brain of patients. The scientist could also identify their composition: They turned out to be dipeptid-repeat proteins, which comprise a very large number of identical building blocks.

“These are very extraordinary proteins that usually don’t show-up in the organism,” Edbauer notes. “As far as we know, they are completely useless and scarcely soluble. Therefore, they tend to aggregate and seem to damage the nerve cells. We haven’t formally proven toxicity, but there is ample evidence.” Because of their peculiarity these proteins might be an interesting target for new therapies. “As the mechanism of their production is so unusual, we may find ways to inhibit their synthesis without interfering with the formation of other proteins. One could also try to block their aggregation and accelerate their decomposition.”

The scientists have applied for a patent and are pursuing a major goal. “At the DZNE in Munich it is our dream to develop a therapy against these devastating diseases,“ Haass and Edbauer conclude.

Filed under neurodegenerative diseases dementia alzheimer's disease genetics neuroscience science

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Researchers identify potential target for age-related cognitive decline Cognitive decline in old age is linked to decreasing production of new neurons. Scientists from the German Cancer Research Center have discovered in mice that significantly more neurons are generated in the brains of older animals if a signaling molecule called Dickkopf-1 is turned off. In tests for spatial orientation and memory, mice in advanced adult age whose Dickkopf gene had been silenced reached an equal mental performance as young animals. The hippocampus – a structure of the brain whose shape resembles that of a seahorse – is also called the “gateway” to memory. This is where information is stored and retrieved. Its performance relies on new neurons being continually formed in the hippocampus over the entire lifetime. “However, in old age, production of new neurons dramatically decreases. This is considered to be among the causes of declining memory and learning ability”, Prof. Dr. Ana Martin-Villalba, a neuroscientist, explains. Martin-Villalba, who heads a research department at the German Cancer Research Center (DKFZ), and her team are trying to find the molecular causes for this decrease in new neuron production (neurogenesis). Neural stem cells in the hippocampus are responsible for continuous supply of new neurons. Specific molecules in the immediate environment of these stem cells determine their fate: They may remain dormant, renew themselves, or differentiate into one of two types of specialized brain cells, astrocytes or neurons. One of these factors is the Wnt signaling molecule, which promotes the formation of young neurons. However, its molecular counterpart, called Dickkopf-1, can prevent this. "We find considerably more Dickkopf-1 protein in the brains of older mice than in those of young animals. We therefore suspected this signaling molecule to be responsible for the fact that hardly any young neurons are generated any more in old age." The scientists tested their assumption in mice whose Dickkopf-1 gene is permanently silenced. Professor Christof Niehrs had developed these animals at DKFZ. The term "Dickkopf" (from German "dick" = thick, "Kopf" = head) also goes back to Niehrs, who had found in 1998 that this signaling molecule regulates head development during embryogenesis.

Researchers identify potential target for age-related cognitive decline

Cognitive decline in old age is linked to decreasing production of new neurons. Scientists from the German Cancer Research Center have discovered in mice that significantly more neurons are generated in the brains of older animals if a signaling molecule called Dickkopf-1 is turned off. In tests for spatial orientation and memory, mice in advanced adult age whose Dickkopf gene had been silenced reached an equal mental performance as young animals.

The hippocampus – a structure of the brain whose shape resembles that of a seahorse – is also called the “gateway” to memory. This is where information is stored and retrieved. Its performance relies on new neurons being continually formed in the hippocampus over the entire lifetime. “However, in old age, production of new neurons dramatically decreases. This is considered to be among the causes of declining memory and learning ability”, Prof. Dr. Ana Martin-Villalba, a neuroscientist, explains.

Martin-Villalba, who heads a research department at the German Cancer Research Center (DKFZ), and her team are trying to find the molecular causes for this decrease in new neuron production (neurogenesis). Neural stem cells in the hippocampus are responsible for continuous supply of new neurons. Specific molecules in the immediate environment of these stem cells determine their fate: They may remain dormant, renew themselves, or differentiate into one of two types of specialized brain cells, astrocytes or neurons. One of these factors is the Wnt signaling molecule, which promotes the formation of young neurons. However, its molecular counterpart, called Dickkopf-1, can prevent this.

"We find considerably more Dickkopf-1 protein in the brains of older mice than in those of young animals. We therefore suspected this signaling molecule to be responsible for the fact that hardly any young neurons are generated any more in old age." The scientists tested their assumption in mice whose Dickkopf-1 gene is permanently silenced. Professor Christof Niehrs had developed these animals at DKFZ. The term "Dickkopf" (from German "dick" = thick, "Kopf" = head) also goes back to Niehrs, who had found in 1998 that this signaling molecule regulates head development during embryogenesis.

Filed under aging cognitive decline memory hippocampus Dickkopf gene neurogenesis neuroscience science

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Million dollar B.R.A.I.N. Prize applications open until March 15, 2013

If you have an exciting advancement in neurotechnology, a million dollar award could help take your product from great idea to world-changing application. Israel Brain Technologies (IBT), a non-profit organization dedicated to the development of brain-related science, is now seeking applicants for its $1,000,000 Global B.R.A.I.N. Prize competition. Applications will be accepted until March 15, 2013.

The Global B.R.A.I.N (Breakthrough Research And Innovation in Neurotechnology) Prize is an international award that was announced in 2011 to be granted to an individual, group or organization for a recent breakthrough in the field of brain technology.

The goal of the prize is best described by Dr. Rafi Gidron, Founder and current Chairman of IBT: “The B.R.A.I.N. Prize will bring together the best minds across geographic boundaries to create the next generation of brain-related innovation, from Brain Machine Interface to Brain Inspired Computing to urgently-needed solutions for brain disease. It’s a global brain-gain. Our aim is to open minds… quite literally.”

The international judging committee for the Global B.R.A.I.N. Prize is composed of distinguished leaders in neuroscience, technology and business, including three Nobel laureates: Profs. Eric Kandel, Daniel Kahneman and Bert Sakmann. IBT is a non-profit organization inspired by the vision of Israeli President Shimon Peres to foster the next global breakthrough in neurotechnology.

Filed under brain B.R.A.I.N. Prize neurotechnology neuroscience technology science

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Number of People with Alzheimer’s Disease May Triple by 2050 The number of people with Alzheimer’s disease is expected to triple in the next 40 years, according to a new study by researchers from Rush University Medical Center published in the February 6, 2013, online issue of Neurology, the medical journal of the American Academy of Neurology. “This increase is due to an aging baby boom generation. It will place a huge burden on society, disabling more people who develop the disease, challenging their caregivers, and straining medical and social safety nets,” said co-author, Jennifer Weuve, MPH, ScD, assistant professor of medicine, Rush Institute for Healthy Aging at Rush University Medical Center in Chicago. “Our study draws attention to an urgent need for more research, treatments and preventive strategies to reduce the impact of this epidemic.” For the study, researchers analyzed information from 10,802 African-American and Caucasian people living in Chicago, ages 65 and older between 1993 and 2011. Participants were interviewed and assessed for dementia every three years. Age, race and level of education were factored into the research. The data was combined with U.S. death rates, education and current and future population estimates from the U.S. Census Bureau. The study found that the total number of people with Alzheimer’s dementia in 2050 is projected to be 13.8 million, up from 4.7 million in 2010. About 7 million of those with the disease would be age 85 or older in 2050. “Our projections use sophisticated methods and the most up-to-date data, but they echo projections made years and decades ago. All of these projections anticipate a future with a dramatic increase in the number of people with Alzheimer’s and should compel us to prepare for it,” said Weuve.

Number of People with Alzheimer’s Disease May Triple by 2050

The number of people with Alzheimer’s disease is expected to triple in the next 40 years, according to a new study by researchers from Rush University Medical Center published in the February 6, 2013, online issue of Neurology, the medical journal of the American Academy of Neurology.

“This increase is due to an aging baby boom generation. It will place a huge burden on society, disabling more people who develop the disease, challenging their caregivers, and straining medical and social safety nets,” said co-author, Jennifer Weuve, MPH, ScD, assistant professor of medicine, Rush Institute for Healthy Aging at Rush University Medical Center in Chicago. “Our study draws attention to an urgent need for more research, treatments and preventive strategies to reduce the impact of this epidemic.”

For the study, researchers analyzed information from 10,802 African-American and Caucasian people living in Chicago, ages 65 and older between 1993 and 2011. Participants were interviewed and assessed for dementia every three years. Age, race and level of education were factored into the research.

The data was combined with U.S. death rates, education and current and future population estimates from the U.S. Census Bureau.

The study found that the total number of people with Alzheimer’s dementia in 2050 is projected to be 13.8 million, up from 4.7 million in 2010. About 7 million of those with the disease would be age 85 or older in 2050.

“Our projections use sophisticated methods and the most up-to-date data, but they echo projections made years and decades ago. All of these projections anticipate a future with a dramatic increase in the number of people with Alzheimer’s and should compel us to prepare for it,” said Weuve.

Filed under alzheimer's disease dementia memory cognitive decline medicine science

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