Neuroscience

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Posts tagged alzheimer's disease

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Can Certain Herbs Stave Off Alzheimer’s Disease? Enhanced extracts made from special antioxidants in spearmint and rosemary improve learning and memory, a study in an animal model at Saint Louis University found. "We found that these proprietary compounds reduce deficits caused by mild cognitive impairment, which can be a precursor to Alzheimer’s disease," said Susan Farr, Ph.D., research professor geriatrics at Saint Louis University School of Medicine. Farr added, “This probably means eating spearmint and rosemary is good for you. However, our experiments were in an animal model and I don’t know how much — or if any amount — of these herbs people would have to consume for learning and memory to improve. In other words, I’m not suggesting that people chew more gum at this point.” Farr presented the early findings at Neuroscience 2013, a meeting of 32,000 on Monday, Nov. 11. She tested a novel antioxidant-based ingredient made from spearmint extract and two different doses of a similar antioxidant made from rosemary extract on mice that have age-related cognitive decline. She found that the higher dose rosemary extract compound was the most powerful in improving memory and learning in three tested behaviors. The lower dose rosemary extract improved memory in two of the behavioral tests, as did the compound made from spearmint extract. Further, there were signs of reduced oxidative stress, which is considered a hallmark of age-related decline, in the part of the brain that controls learning and memory. "Our research suggests these extracts made from herbs might have beneficial effects on altering the course of age-associated cognitive decline," Farr said. "It’s worth additional study." (Image credit)

Can Certain Herbs Stave Off Alzheimer’s Disease?

Enhanced extracts made from special antioxidants in spearmint and rosemary improve learning and memory, a study in an animal model at Saint Louis University found.

"We found that these proprietary compounds reduce deficits caused by mild cognitive impairment, which can be a precursor to Alzheimer’s disease," said Susan Farr, Ph.D., research professor geriatrics at Saint Louis University School of Medicine.

Farr added, “This probably means eating spearmint and rosemary is good for you. However, our experiments were in an animal model and I don’t know how much — or if any amount — of these herbs people would have to consume for learning and memory to improve. In other words, I’m not suggesting that people chew more gum at this point.”

Farr presented the early findings at Neuroscience 2013, a meeting of 32,000 on Monday, Nov. 11. She tested a novel antioxidant-based ingredient made from spearmint extract and two different doses of a similar antioxidant made from rosemary extract on mice that have age-related cognitive decline.

She found that the higher dose rosemary extract compound was the most powerful in improving memory and learning in three tested behaviors. The lower dose rosemary extract improved memory in two of the behavioral tests, as did the compound made from spearmint extract.

Further, there were signs of reduced oxidative stress, which is considered a hallmark of age-related decline, in the part of the brain that controls learning and memory.

"Our research suggests these extracts made from herbs might have beneficial effects on altering the course of age-associated cognitive decline," Farr said. "It’s worth additional study."

(Image credit)

Filed under alzheimer's disease cognitive decline rosemary spearmint Neuroscience 2013 neuroscience science

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New Compound Inhibits Cognitive Impairment in Animal Models of Alzheimer’s Disease

The novel compound IRL-1620 may be useful in treating Alzheimer’s disease (AD) as it has been shown to prevent cognitive impairment and oxidative stress in animal models. This research is being presented at the 2013 American Association of Pharmaceutical Scientists (AAPS) Annual Meeting and Exposition, the world’s largest pharmaceutical sciences meeting, in San Antonio, Nov. 10–14.

AD is a form of dementia that worsens over time, leading to a slow decline in cognitive functions and affecting memory, thinking, and behavior. More than 5 million Americans are living with AD, according to the Alzheimer’s Association.

Anil Gulati, M.D., Ph.D., FCP, and Seema Briyal, Ph.D., along with their colleagues from Midwestern University, administered Amyloid beta (Aβ), a main component of certain deposits located in AD patients’ brains, to normal and diabetic rats on days 1, 7, and 14. Spatial learning and memory were tested in a Morris water maze. The pool was divided into four equal quadrants, and an escape platform was hidden below the surface at a fixed location in one of the quadrants.

The rats had to find the platform within 60 seconds. The average time it took on day 4 for Aβ-treated rats to locate the platform was 55.05 seconds, though a majority of this group was not able to find it in the designated time. Aβ rats treated with IRL-1620 were able to locate the platform in 26.53 seconds, nearly half the time. After five days, Aβ rats treated with IRL-1620 showed a 60 percent improvement in learning and memory.

“Our research is based on the idea of using the Endothelin (ET) system in the treatment of AD,” said Gulati. “The ET system is traditionally known to play a role in the regulation of blood flow. This is important in the potential treatment of AD since disturbances in blood flow could damage the brain’s ability to clear damaging particles, leading to a build-up of toxic substances and cognitive impairment.”

The next stage of Gulati’s research is to further investigate the endothelin receptor type B’s mechanisms of neuroprotection and to look into possible resulting tissue changes following AD.

The FDA has approved five medications to treat the symptoms of AD. Current drugs help mask the symptoms but do not treat the underlying disease. A breakthrough Alzheimer’s treatment would target the underlying disease and stop or delay the cell damage that eventually leads to the worsening of symptoms.

(Source: newswise.com)

Filed under alzheimer's disease dementia beta amyloid IRL-1620 endothelin neuroscience science

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Can the Eyes Help Diagnose Alzheimer’s Disease? An international team of researchers studying the link between vision loss and Alzheimer’s disease report that the loss of a particular layer of retinal cells not previously investigated may reveal the disease’s presence and provide a new way to track disease progression. The researchers, from Georgetown University Medical Center (GUMC) and the University of Hong Kong, examined retinas from the eyes of mice genetically engineered to develop Alzheimer’s disease (AD). They presented their findings today at Neuroscience 2013, the annual meeting of the Society for Neuroscience. “The retina is an extension of the brain so it makes sense to see if the same pathologic processes found in an Alzheimer’s brain are also found in the eye,” explains R. Scott Turner, MD, PhD, director of the Memory Disorders Program at GUMC and the only U.S. author on the study. “We know there’s an association between glaucoma and Alzheimer’s in that both are characterized by loss of neurons, but the mechanisms are not clear.”  Turner says many researchers increasingly view glaucoma as a neurodegenerative disorder similar to AD. Most of the research to date examining the relationship between glaucoma and Alzheimer’s focused on the retinal ganglion cell layer, which transmits visual information via the optic nerve into the brain. Before that transmission happens, though, the retinal ganglion cells receive information from another layer in the retina called the inner nuclear layer. In their study, the researchers looked at the thickness of the retina, including the inner nuclear layer (not previously study in this setting) and the retinal ganglion cell layer.  They found a significant loss of thickness in both. The inner nuclear layer had a 37 percent loss of neurons and the retinal ganglion cell layer a 49 percent loss, compared with healthy, age-matched control mice. In humans, the structure and thickness of the retina can be readily measured using optical coherence tomography.  Turner says this new tool is increasing finding applications in research and clinical care.  “This study suggests another path forward in understanding the disease process and could lead to new ways to diagnose or predict Alzheimer’s that could be as simple as looking into the eyes,” Turner says. “Parallel disease mechanisms suggest that new treatments developed for Alzheimer’s may also be useful for glaucoma.”

Can the Eyes Help Diagnose Alzheimer’s Disease?

An international team of researchers studying the link between vision loss and Alzheimer’s disease report that the loss of a particular layer of retinal cells not previously investigated may reveal the disease’s presence and provide a new way to track disease progression.

The researchers, from Georgetown University Medical Center (GUMC) and the University of Hong Kong, examined retinas from the eyes of mice genetically engineered to develop Alzheimer’s disease (AD). They presented their findings today at Neuroscience 2013, the annual meeting of the Society for Neuroscience.

“The retina is an extension of the brain so it makes sense to see if the same pathologic processes found in an Alzheimer’s brain are also found in the eye,” explains R. Scott Turner, MD, PhD, director of the Memory Disorders Program at GUMC and the only U.S. author on the study. “We know there’s an association between glaucoma and Alzheimer’s in that both are characterized by loss of neurons, but the mechanisms are not clear.” 

Turner says many researchers increasingly view glaucoma as a neurodegenerative disorder similar to AD.

Most of the research to date examining the relationship between glaucoma and Alzheimer’s focused on the retinal ganglion cell layer, which transmits visual information via the optic nerve into the brain. Before that transmission happens, though, the retinal ganglion cells receive information from another layer in the retina called the inner nuclear layer.

In their study, the researchers looked at the thickness of the retina, including the inner nuclear layer (not previously study in this setting) and the retinal ganglion cell layer.  They found a significant loss of thickness in both. The inner nuclear layer had a 37 percent loss of neurons and the retinal ganglion cell layer a 49 percent loss, compared with healthy, age-matched control mice.

In humans, the structure and thickness of the retina can be readily measured using optical coherence tomography.  Turner says this new tool is increasing finding applications in research and clinical care. 

“This study suggests another path forward in understanding the disease process and could lead to new ways to diagnose or predict Alzheimer’s that could be as simple as looking into the eyes,” Turner says. “Parallel disease mechanisms suggest that new treatments developed for Alzheimer’s may also be useful for glaucoma.”

Filed under alzheimer's disease vision loss retinal cells glaucoma Neuroscience 2013 neuroscience science

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High Blood Pressure in Middle Age Versus Old Age May Better Predict Memory Loss

People in middle age who have a high blood pressure measure called pulse pressure are more likely to have biomarkers of Alzheimer’s disease in their spinal fluid than those with lower pulse pressure, according to research published in the November 13, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

Pulse pressure is the systolic pressure, or the top number in a blood pressure reading, minus the diastolic, or the bottom number. Pulse pressure increases with age and is an index of the aging of the vascular system.

The study involved 177 people ages 55 to 100 with no symptoms of Alzheimer’s disease. Participants had their pulse pressure taken and lumbar punctures to obtain spinal fluid.

The study found that people who have higher pulse pressure are more likely to have the Alzheimer’s biomarkers amyloid beta, or plaques, and p-tau protein, or tangles, in their cerebral spinal fluid than those with lower pulse pressure. For every 10 point rise in pulse pressure, the average level of p-tau protein in the spinal fluid rose by 1.5 picograms per millileter. A picogram is one trillionth of a gram.

“These results suggest that the forces involved in blood circulation may be related to the development of the hallmark Alzheimer’s disease signs that cause loss of brain cells,” said study author Daniel A. Nation, PhD, of the VA San Diego Healthcare System.

The relationship was found in people age 55 to 70, but not in people age 70 to 100.

“This is consistent with findings indicating that high blood pressure in middle age is a better predictor of later problems with memory and thinking skills and loss of brain cells than high blood pressure in old age,” Nation said.

Filed under alzheimer's disease dementia beta amyloid neurodegeneration blood pressure neuroscience science

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Study Examines Amyloid Deposition in Patients with Traumatic Brain Injury

Patients with traumatic brain injury (TBI) had increased deposits of β-Amyloid (Αβ) plaques, a hallmark of Alzheimer Disease (AD), in some areas of their brains in a study by Young T. Hong, Ph.D., of the University of Cambridge, England, and colleagues.

There may be epidemiological or pathophysiological (changes because of injury) links between TBI and AD, and Αβ plaques are found in as many as 30 percent of patients who die in the acute phase after a TBI. The plaques appear within hours of the injury and can occur in patients of all ages, according to the study background.

Researchers used imaging and brain tissue acquired during autopsies to examine Αβ deposition in patients with TBI. Researchers performed positron emission tomography (PET) imaging using carbon 11-labeled Pittsburgh Compound B ([11C]PIB), a marker of brain amyloid deposition, in 15 participants with a TBI and 11 healthy patients. Autopsy-acquired brain tissue was obtained from 16 people who had a TBI, as well as seven patients with a nonneurological cause of death.

The study’s findings indicate that patients with TBI showed increases in [11C]PIB binding, which may be a marker of Αβ plaque in some areas of the brain.

“The use of ([11C]PIB PET for amyloid imaging following TBI provides us with the potential for understanding the pathophysiology of TBI, for characterizing the mechanistic drivers of disease progression or suboptimal recovery in the subacute phase of TBI, for identifying patients at high risk of accelerated AD, and for evaluating the potential of antiamyloid therapies,” the authors conclude.

(Source: media.jamanetwork.com)

Filed under TBI brain injury beta amyloid alzheimer's disease neuroscience science

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Signal found to enhance survival of new brain cells A specialized type of brain cell that tamps down stem cell activity ironically, perhaps, encourages the survival of the stem cells’ progeny, Johns Hopkins researchers report. Understanding how these new brain cells “decide” whether to live or die and how to behave is of special interest because changes in their activity are linked to neurodegenerative diseases such as Alzheimer’s, mental illness and aging. "We’ve identified a critical mechanism for keeping newborn neurons, or new brain cells, alive," says Hongjun Song, Ph.D., professor of neurology and director of Johns Hopkins Medicine’s Institute for Cell Engineering’s Stem Cell Program. "Not only can this help us understand the underlying causes of some diseases, it may also be a step toward overcoming barriers to therapeutic cell transplantation." Working with a group led by Guo-li Ming, M.D., Ph.D., a professor of neurology in the Institute for Cell Engineering, and other collaborators, Song’s research team first reported last year that brain cells known as parvalbumin-expressing interneurons instruct nearby stem cells not to divide by releasing a chemical signal called GABA. In their new study, as reported Nov. 10 online in Nature Neuroscience, Song and Ming wanted to find out how GABA from surrounding neurons affects the newborn neurons that stem cells produce. Many of these newborn neurons naturally die soon after their “birth,” Song says; if they do survive, the new cells migrate to a permanent home in the brain and forge connections called synapses with other cells. To learn whether GABA is a factor in the newborn neurons’ survival and behavior, the research team tagged newborn neurons from mouse brains with a fluorescent protein, then watched their response to GABA. “We didn’t expect these immature neurons to form synapses, so we were surprised to see that they had built synapses from surrounding interneurons and that GABA was getting to them that way,” Song says. In the earlier study, the team had found that GABA was getting to the synapse-less stem cells by a less direct route, drifting across the spaces between cells. To confirm the finding, the team engineered the interneurons to be either stimulated or suppressed by light. When stimulated, the cells would indeed activate nearby newborn neurons, the researchers found. They next tried the light-stimulation trick in live mice, and found that when the specialized interneurons were stimulated and gave off more GABA, the mice’s newborn neurons survived in greater numbers than otherwise. This was in contrast to the response of the stem cells, which go dormant when they detect GABA. "This appears to be a very efficient system for tuning the brain’s response to its environment," says Song. "When you have a high level of brain activity, you need more newborn neurons, and when you don’t have high activity, you don’t need newborn neurons, but you need to prepare yourself by keeping the stem cells active. It’s all regulated by the same signal." Song notes that parvalbumin-expressing interneurons have been found by others to behave abnormally in neurodegenerative diseases such as Alzheimer’s and mental illnesses such as schizophrenia. “Now we want to see what the role of these interneurons is in the newborn neurons’ next steps: migrating to the right place and integrating into the existing circuitry,” he says. “That may be the key to their role in disease.” The team is also interested in investigating whether the GABA mechanism can be used to help keep transplanted cells alive without affecting other brain processes as a side effect.

Signal found to enhance survival of new brain cells

A specialized type of brain cell that tamps down stem cell activity ironically, perhaps, encourages the survival of the stem cells’ progeny, Johns Hopkins researchers report. Understanding how these new brain cells “decide” whether to live or die and how to behave is of special interest because changes in their activity are linked to neurodegenerative diseases such as Alzheimer’s, mental illness and aging.

"We’ve identified a critical mechanism for keeping newborn neurons, or new brain cells, alive," says Hongjun Song, Ph.D., professor of neurology and director of Johns Hopkins Medicine’s Institute for Cell Engineering’s Stem Cell Program. "Not only can this help us understand the underlying causes of some diseases, it may also be a step toward overcoming barriers to therapeutic cell transplantation."

Working with a group led by Guo-li Ming, M.D., Ph.D., a professor of neurology in the Institute for Cell Engineering, and other collaborators, Song’s research team first reported last year that brain cells known as parvalbumin-expressing interneurons instruct nearby stem cells not to divide by releasing a chemical signal called GABA.

In their new study, as reported Nov. 10 online in Nature Neuroscience, Song and Ming wanted to find out how GABA from surrounding neurons affects the newborn neurons that stem cells produce. Many of these newborn neurons naturally die soon after their “birth,” Song says; if they do survive, the new cells migrate to a permanent home in the brain and forge connections called synapses with other cells.

To learn whether GABA is a factor in the newborn neurons’ survival and behavior, the research team tagged newborn neurons from mouse brains with a fluorescent protein, then watched their response to GABA. “We didn’t expect these immature neurons to form synapses, so we were surprised to see that they had built synapses from surrounding interneurons and that GABA was getting to them that way,” Song says. In the earlier study, the team had found that GABA was getting to the synapse-less stem cells by a less direct route, drifting across the spaces between cells.

To confirm the finding, the team engineered the interneurons to be either stimulated or suppressed by light. When stimulated, the cells would indeed activate nearby newborn neurons, the researchers found. They next tried the light-stimulation trick in live mice, and found that when the specialized interneurons were stimulated and gave off more GABA, the mice’s newborn neurons survived in greater numbers than otherwise. This was in contrast to the response of the stem cells, which go dormant when they detect GABA.

"This appears to be a very efficient system for tuning the brain’s response to its environment," says Song. "When you have a high level of brain activity, you need more newborn neurons, and when you don’t have high activity, you don’t need newborn neurons, but you need to prepare yourself by keeping the stem cells active. It’s all regulated by the same signal."

Song notes that parvalbumin-expressing interneurons have been found by others to behave abnormally in neurodegenerative diseases such as Alzheimer’s and mental illnesses such as schizophrenia. “Now we want to see what the role of these interneurons is in the newborn neurons’ next steps: migrating to the right place and integrating into the existing circuitry,” he says. “That may be the key to their role in disease.” The team is also interested in investigating whether the GABA mechanism can be used to help keep transplanted cells alive without affecting other brain processes as a side effect.

Filed under alzheimer's disease interneurons hippocampus schizophrenia stem cells synapses neuroscience science

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New Method Predicts Time from Alzheimer’s Onset to Nursing Home, Death

A Columbia University Medical Center-led research team has clinically validated a new method for predicting time to full-time care, nursing home residence, or death for patients with Alzheimer’s disease. The method, which uses data gathered from a single patient visit, is based on a complex model of Alzheimer’s disease progression that the researchers developed by consecutively following two sets of Alzheimer’s patients for 10 years each. The results were published online ahead of print in the Journal of Alzheimer’s Disease.

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“Predicting Alzheimer’s progression has been a challenge because the disease varies significantly from one person to another—two Alzheimer’s patients may both appear to have mild forms of the disease, yet one may progress rapidly, while the other progresses much more slowly,” said senior author Yaakov Stern, PhD, professor of neuropsychology (in neurology, psychiatry, and psychology and in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain and the Gertrude H. Sergievsky Center) at CUMC. “Our method enables clinicians to predict the disease path with great specificity.”

(Source: newsroom.cumc.columbia.edu)

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Filed under alzheimer's disease dementia neurodegeneration neuroscience science

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Speaking another language may delay dementia A team of scientists examined almost 650 dementia patients and assessed when each one had been diagnosed with the condition. The study was carried out by researchers from the University and Nizam’s Institute of Medical Sciences in Hyderabad (India). Bilingual advantage They found that people who spoke two or more languages experienced a later onset of Alzheimer’s disease, vascular dementia and frontotemporal dementia. The bilingual advantage extended to illiterate people who had not attended school. This confirms that the observed effect is not caused by differences in formal education. It is the largest study so far to gauge the impact of bilingualism on the onset of dementia - independent of a person’s education, gender, occupation and whether they live in a city or in the country, all of which have been examined as potential factors influencing the onset of dementia. Natural brain training The team of researchers say further studies are needed to determine the mechanism, which causes the delay in the onset of dementia. The researchers suggest that bilingual switching between different sounds, words, concepts, grammatical structures and social norms constitutes a form of natural brain training, likely to be more effective than any artificial brain training programme. However, studies of bilingualism are complicated by the fact that bilingual populations are often ethnically and culturally different from monolingual societies. India offers in this respect a unique opportunity for research. In places like Hyderabad, bilingualism is part of everyday life: knowledge of several languages is the norm and monolingualism an exception. These findings suggest that bilingualism might have a stronger influence on dementia that any currently available drugs. This makes the study of the relationship between bilingualism and cognition one of our highest priorities. -Thomas Bak, School of Philosophy, Psychology and Language Sciences The study, published in Neurology, the medical journal of the American Academy of Neurology, was supported by the Indian Department of Science and Technology and by the Centre for Cognitive Aging and Cognitive Epidemiology (CCACE) at the University of Edinburgh. It was led by Suvarna Alladi, DM, at the Nizam’s Institute of Medical Sciences in Hyderabad.

Speaking another language may delay dementia

A team of scientists examined almost 650 dementia patients and assessed when each one had been diagnosed with the condition. The study was carried out by researchers from the University and Nizam’s Institute of Medical Sciences in Hyderabad (India).

Bilingual advantage

They found that people who spoke two or more languages experienced a later onset of Alzheimer’s disease, vascular dementia and frontotemporal dementia.

The bilingual advantage extended to illiterate people who had not attended school. This confirms that the observed effect is not caused by differences in formal education.

It is the largest study so far to gauge the impact of bilingualism on the onset of dementia - independent of a person’s education, gender, occupation and whether they live in a city or in the country, all of which have been examined as potential factors influencing the onset of dementia.

Natural brain training

The team of researchers say further studies are needed to determine the mechanism, which causes the delay in the onset of dementia. The researchers suggest that bilingual switching between different sounds, words, concepts, grammatical structures and social norms constitutes a form of natural brain training, likely to be more effective than any artificial brain training programme.

However, studies of bilingualism are complicated by the fact that bilingual populations are often ethnically and culturally different from monolingual societies. India offers in this respect a unique opportunity for research. In places like Hyderabad, bilingualism is part of everyday life: knowledge of several languages is the norm and monolingualism an exception.

These findings suggest that bilingualism might have a stronger influence on dementia that any currently available drugs. This makes the study of the relationship between bilingualism and cognition one of our highest priorities. -Thomas Bak, School of Philosophy, Psychology and Language Sciences

The study, published in Neurology, the medical journal of the American Academy of Neurology, was supported by the Indian Department of Science and Technology and by the Centre for Cognitive Aging and Cognitive Epidemiology (CCACE) at the University of Edinburgh. It was led by Suvarna Alladi, DM, at the Nizam’s Institute of Medical Sciences in Hyderabad.

Filed under alzheimer's disease dementia neurodegeneration language bilingualism neuroscience science

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Brain aging is conclusively linked to genes; a crucial first step in finding biological mechanisms of normal aging

For the first time in a large study sample, the decline in brain function in normal aging is conclusively shown to be influenced by genes, say researchers from the Texas Biomedical Research Institute and Yale University.

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“Identification of genes associated with brain aging should improve our understanding of the biological processes that govern normal age-related decline,” said John Blangero, Ph.D., a Texas Biomed geneticist and the senior author of the paper. The study, funded by the National Institutes of Health (NIH),  is published in the November 4, 2013 issue of the Proceedings of the National Academy of Sciences. David Glahn, Ph.D., an associate professor of psychiatry at the Yale University School of Medicine, is the first author on the paper.

In large pedigrees including 1,129 people aged 18 to 83, the scientists documented profound aging effects from young adulthood to old age, on neurocognitive ability and brain white matter measures. White matter actively affects how the brain learns and functions. Genetic material shared amongst biological relatives appears to predict the observed changes in brain function with age.

Participants were enrolled in the Genetics of Brain Structure and Function Study and drawn from large Mexican Americans families in San Antonio. Brain imaging studies were conducted at the University of Texas Health Science Center at San Antonio Research Imaging Institute  directed by  Peter Fox, M.D.

“The use of large human pedigrees provides a powerful resource for measuring how genetic factors change with age,” Blangero said.

By applying a sophisticated analysis, the scientists demonstrated a heritable basis for neurocognitive deterioration with age that could be attributed to genetic factors. Similarly, decreasing white matter integrity with age was influenced by genes., The investigators further demonstrated that different sets of genes are responsible for these two biological aging processes.

 “A key advantage of this study is that we specifically focused on large extended families and so we were able to disentangle genetic from non-genetic influences on the aging process,” said Glahn.

(Source: txbiomed.org)

Filed under aging white matter alzheimer's disease dementia brain mapping neuroscience science

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Lasers might be the cure for brain diseases such as Alzheimer’s and Parkinson’s Researchers at Chalmers University of Technology in Sweden, together with researchers at the Polish Wroclaw University of Technology, have made a discovery that may lead to the curing of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease (the so called mad cow disease) through photo therapy. The researchers discovery, which was published yesterday in the journal Nature Photonics, is that it is possible to distinguish aggregations of the proteins, believed to cause the diseases, from the the well-functioning proteins in the body by using multi-photon laser technique. “Nobody has talked about using only light to treat these diseases until now. This is a totally new approach and we believe that this might become a breakthrough in the research of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease. We have found a totally new way of discovering these structures using just laser light”, says Piotr Hanczyc at Chalmers University of Technology. If the protein aggregates are removed, the disease is in principle cured. The problem until now has been to detect and remove the aggregates. The researchers now harbor high hopes that photo acoustic therapy, which is already used for tomography, may be used to remove the malfunctioning proteins. Today amyloid protein aggregates are treated with chemicals, both for detection as well as removal. These chemicals are highly toxic and harmful for those treated. With multi photon laser the chemical treatment would be unnecessary. Nor would surgery be necessary for removing of aggregates. Due to this discovery it might, thus, be possible to remove the harmful protein without touching the surrounding tissue. These diseases arise when amyloid beta protein are aggregated in large doses so they start to inhibit proper cellular processes. Different proteins create different kinds of amyloids, but they generally have the same structure. This makes them different from the well-functioning proteins in the body, which can now be shown by multi photon laser technique.

Lasers might be the cure for brain diseases such as Alzheimer’s and Parkinson’s

Researchers at Chalmers University of Technology in Sweden, together with researchers at the Polish Wroclaw University of Technology, have made a discovery that may lead to the curing of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease (the so called mad cow disease) through photo therapy.

The researchers discovery, which was published yesterday in the journal Nature Photonics, is that it is possible to distinguish aggregations of the proteins, believed to cause the diseases, from the the well-functioning proteins in the body by using multi-photon laser technique.

“Nobody has talked about using only light to treat these diseases until now. This is a totally new approach and we believe that this might become a breakthrough in the research of diseases such as Alzheimer’s, Parkinson’s and Creutzfeldt-Jakob disease. We have found a totally new way of discovering these structures using just laser light”, says Piotr Hanczyc at Chalmers University of Technology.

If the protein aggregates are removed, the disease is in principle cured. The problem until now has been to detect and remove the aggregates.

The researchers now harbor high hopes that photo acoustic therapy, which is already used for tomography, may be used to remove the malfunctioning proteins. Today amyloid protein aggregates are treated with chemicals, both for detection as well as removal. These chemicals are highly toxic and harmful for those treated.

With multi photon laser the chemical treatment would be unnecessary. Nor would surgery be necessary for removing of aggregates. Due to this discovery it might, thus, be possible to remove the harmful protein without touching the surrounding tissue.

These diseases arise when amyloid beta protein are aggregated in large doses so they start to inhibit proper cellular processes.

Different proteins create different kinds of amyloids, but they generally have the same structure. This makes them different from the well-functioning proteins in the body, which can now be shown by multi photon laser technique.

Filed under alzheimer's disease parkinson's disease Creutzfeldt-Jakob disease multi-photon laser amyloid protein science

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