Biotechia

neurosciencestuff:

Today the White House announced its goal to fund Brain Research, in hopes of furthering understanding of brain disorders and degenerative diseases such as Alzheimer’s.

Two years ago Scientific American magazine sent me to the University of Texas at Austin to borrow a human brain. They needed me to photograph a normal, adult, non-dissected brain that the university had obtained by trading a syphilitic lung with another institution. The specimen was waiting for me, but before I left they asked if I’d like to see their collection.

I walked into a storage closet filled with approximately one-hundred human brains, none of them normal, taken from patients at the Texas State Mental Hospital. The brains sat in large jars of fluid, each labeled with a date of death or autopsy, a brief description in Latin, and a case number. These case numbers corresponded to micro film held by the State Hospital detailing medical histories. But somehow, regardless of how amazing and fascinating this collection was, it had been largely untouched, and unstudied for nearly three decades.

Driving back to my studio with a brain snugly belted into the passenger seat, I quickly became obsessed with the idea of photographing the collection, preserving the already decaying brains, and corresponding the images to their medical histories. I met with my friend Alex Hannaford, a features journalist, to help me find the collection’s history dating back to the 1950s.

Over the past year while working this idea into a book, we’ve learned how heavily storied the collection is. That it was originally intended to be displayed and studied, but without funding it instead stagnated. And that the microfilm histories of each brain had been destroyed years ago.

My original vision of a photo book accompanied by medical data and a comprehensive essay turned into a story of loss and neglect. But Alex continued to pursue some scientific hope for the collection. After discussions with various neuroscientists we learned that through MRI technology and special techniques in DNA scanning there is still hope. And with the new possibilities of federal brain research funding, this collection’s secrets may yet be unlocked.

As we begin the hunt for someone to publish my 230 images accompanied by Alex’s 14,000 word essay, the University has found new interest in the collection. They currently are planning to make MRI scans of the brains.

Malformed – A Collection of Human Brains from the Texas State Mental Hospital by Adam Voorhes

Reblogged from Neuroscience


Genetic markers ID second Alzheimer’s pathway
Researchers at Washington University School of Medicine in St. Louis have identified a new set of genetic markers for Alzheimer’s that point to a second pathway through which the disease develops.
Much of the genetic research on Alzheimer’s centers on amyloid-beta, a key component of brain plaques that build up in the brains of people with the disease. In the new study, the scientists identified several genes linked to the tau protein, which is found in the tangles that develop in the brain as Alzheimer’s progresses and patients develop dementia. The findings may help provide targets for a different class of drugs that could be used for treatment.
The researchers report their findings online April 24 in the journal Neuron.“We measured the tau protein in the cerebrospinal fluid and identified several genes that are related to high levels of tau and also affect risk for Alzheimer’s disease,” says senior investigator Alison M. Goate, DPhil, the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry. “As far as we’re aware, three of these genes have no effect on amyloid-beta, suggesting that they are operating through a completely different pathway.”
A fourth gene in the mix, APOE, had been identified long ago as a risk factor for Alzheimer’s. It has been linked to amyloid-beta, but in the new study,APOE appears to be connected to elevated levels of tau. Finding that APOEis influencing more than one pathway could help explain why the gene has such a big effect on Alzheimer’s disease risk, the researchers say.
“It appears APOE influences risk in more than one way,” says Goate, also a professor of genetics and co-director of the Hope Center for Neurological Disorders. “Some of the effects are mediated through amyloid-beta and others by tau. That suggests there are at least two ways in which the gene can influence our risk for Alzheimer’s disease.”The new research by Goate and her colleagues is the largest genome-wide association study (GWAS) yet on tau in cerebrospinal fluid. The scientists analyzed points along the genomes of 1,269 individuals who had undergone spinal taps as part of ongoing Alzheimer’s research.
Whereas amyloid is known to collect in the brain and affect brain cells from the outside, the tau protein usually is stored inside cells. So tau usually moves into the spinal fluid when cells are damaged or die. Elevated tau has been linked to several forms of non-Alzheimer’s dementia, and first author Carlos Cruchaga, PhD, says that although amyloid plaques are a key feature of Alzheimer’s disease, it’s possible that excess tau has more to do with the dementia than plaques.
“We know there are some individuals with high levels of amyloid-beta who don’t develop Alzheimer’s disease,” says Cruchaga, an assistant professor of psychiatry. “We don’t know why that is, but perhaps it could be related to the fact that they don’t have elevated tau levels.”
In addition to APOE, the researchers found that a gene called GLIS3, and the genes TREM2 andTREML2 also affect both tau levels and Alzheimer’s risk.
Goate says she suspects changes in tau may be good predictors of advancing disease. As tau levels rise, she says people may be more likely to develop dementia. If drugs could be developed to target tau, they may prevent much of the neurodegeneration that characterizes Alzheimer’s disease and, in that way, help prevent or delay dementia.
The new research also suggests it may one day be possible to reduce Alzheimer’s risk by targeting both pathways.
“Since two mechanisms apparently exist, identifying potential drug targets along these pathways could be very useful,” she says. “If drugs that influence tau could be added to those that affect amyloid, we could potentially reduce risk through two different pathways.”
Image:Both a tangle (top left) and a plaque (bottom right) can be seen in the brain of a patient with Alzheimer’s disease.
Credit: NIGEL CAIRNS, PHD
Audio Available here

Genetic markers ID second Alzheimer’s pathway

Researchers at Washington University School of Medicine in St. Louis have identified a new set of genetic markers for Alzheimer’s that point to a second pathway through which the disease develops.

Much of the genetic research on Alzheimer’s centers on amyloid-beta, a key component of brain plaques that build up in the brains of people with the disease. 

In the new study, the scientists identified several genes linked to the tau protein, which is found in the tangles that develop in the brain as Alzheimer’s progresses and patients develop dementia. The findings may help provide targets for a different class of drugs that could be used for treatment.

The researchers report their findings online April 24 in the journal Neuron.

“We measured the tau protein in the cerebrospinal fluid and identified several genes that are related to high levels of tau and also affect risk for Alzheimer’s disease,” says senior investigator Alison M. Goate, DPhil, the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry. “As far as we’re aware, three of these genes have no effect on amyloid-beta, suggesting that they are operating through a completely different pathway.”

A fourth gene in the mix, APOE, had been identified long ago as a risk factor for Alzheimer’s. It has been linked to amyloid-beta, but in the new study,APOE appears to be connected to elevated levels of tau. Finding that APOEis influencing more than one pathway could help explain why the gene has such a big effect on Alzheimer’s disease risk, the researchers say.

“It appears APOE influences risk in more than one way,” says Goate, also a professor of genetics and co-director of the Hope Center for Neurological Disorders. “Some of the effects are mediated through amyloid-beta and others by tau. That suggests there are at least two ways in which the gene can influence our risk for Alzheimer’s disease.”

The new research by Goate and her colleagues is the largest genome-wide association study (GWAS) yet on tau in cerebrospinal fluid. The scientists analyzed points along the genomes of 1,269 individuals who had undergone spinal taps as part of ongoing Alzheimer’s research.

Whereas amyloid is known to collect in the brain and affect brain cells from the outside, the tau protein usually is stored inside cells. So tau usually moves into the spinal fluid when cells are damaged or die. Elevated tau has been linked to several forms of non-Alzheimer’s dementia, and first author Carlos Cruchaga, PhD, says that although amyloid plaques are a key feature of Alzheimer’s disease, it’s possible that excess tau has more to do with the dementia than plaques.

“We know there are some individuals with high levels of amyloid-beta who don’t develop Alzheimer’s disease,” says Cruchaga, an assistant professor of psychiatry. “We don’t know why that is, but perhaps it could be related to the fact that they don’t have elevated tau levels.”

In addition to APOE, the researchers found that a gene called GLIS3, and the genes TREM2 andTREML2 also affect both tau levels and Alzheimer’s risk.

Goate says she suspects changes in tau may be good predictors of advancing disease. As tau levels rise, she says people may be more likely to develop dementia. If drugs could be developed to target tau, they may prevent much of the neurodegeneration that characterizes Alzheimer’s disease and, in that way, help prevent or delay dementia.

The new research also suggests it may one day be possible to reduce Alzheimer’s risk by targeting both pathways.

“Since two mechanisms apparently exist, identifying potential drug targets along these pathways could be very useful,” she says. “If drugs that influence tau could be added to those that affect amyloid, we could potentially reduce risk through two different pathways.”

Image:Both a tangle (top left) and a plaque (bottom right) can be seen in the brain of a patient with Alzheimer’s disease.

Credit: NIGEL CAIRNS, PHD

Audio Available here

Reblogged from Neuromorphogenesis!

neuromorphogenesis:

3-D stem cell culture technique to better understand Alzheimer’s disease
Facilitates development of treatments and cures to Alzheimer’s disease
A team of researchers at The New York Stem Cell Foundation Research Institute led by Scott Noggle, PhD, Director of the NYSCF Laboratory and the NYSCF – Charles Evans Senior Research Fellow for Alzheimer’s Disease, and Michael W. Nestor, PhD, a NYSCF Postdoctoral Research Fellow, has developed a technique to produce three-dimensional cultures of induced pluripotent stem (iPS) cells called embryoid bodies, amenable to live cell imaging and to electrical activity measurement. As reported in their Stem Cell Research study, these cell aggregates enable scientists to both model and to study diseases such as Alzheimer’s and Parkinson’s disease.
The NYSCF Alzheimer’s disease research team aims to better understand and to find treatments to this disease through stem cell research. For such disorders in which neurons misfire or degenerate, the NYSCF team creates “disease in a dish” models by reprogramming patients’ skin and or blood samples into induced pluripotent stem (iPS) cells that can become neurons and the other brain cells affected in the diseases.
The cells in our body form three-dimensional networks, essential to tissue function and overall health; however, previous techniques to form complex brain tissue resulted in structures that, while similar in form to naturally occurring neurons, undermined imaging or electrical recording attempts.
In the current study, the Noggle and Nestor with NYSCF scientists specially adapted two-dimensional culture methods to grow three-dimensional neuron structures from iPS cells. The resultant neurons were “thinned-out,” enabling calcium-imaging studies, which measure the electrical activity of cells like neurons.
“Combining the advantages of iPS cells grown in a 3D environment with those of a 2D system, our technique produces cells that can be used to observe electrical activity of putative networks of biologically active neurons, while simultaneously imaging them,” said Nestor. “This is key to modeling and studying neurodegenerative diseases.”
Neural networks, thought to underlie learning and memory, become disrupted in Alzheimer’s disease. By generating aggregates from iPS cells and comparing these to an actual patient’s brain tissue, scientists may uncover how disease interferes with these cell-to-cell interactions and understand how to intervene to slow or stop Alzheimer’s disease.
“This critical new tool developed by our Alzheimer’s team will accelerate Alzheimer’s research, enabling more accurate manipulation of cells to find a cure to this disease,” said Susan L. Solomon, CEO of NYSCF.

neuromorphogenesis:

3-D stem cell culture technique to better understand Alzheimer’s disease

Facilitates development of treatments and cures to Alzheimer’s disease

A team of researchers at The New York Stem Cell Foundation Research Institute led by Scott Noggle, PhD, Director of the NYSCF Laboratory and the NYSCF – Charles Evans Senior Research Fellow for Alzheimer’s Disease, and Michael W. Nestor, PhD, a NYSCF Postdoctoral Research Fellow, has developed a technique to produce three-dimensional cultures of induced pluripotent stem (iPS) cells called embryoid bodies, amenable to live cell imaging and to electrical activity measurement. As reported in their Stem Cell Research study, these cell aggregates enable scientists to both model and to study diseases such as Alzheimer’s and Parkinson’s disease.

The NYSCF Alzheimer’s disease research team aims to better understand and to find treatments to this disease through stem cell research. For such disorders in which neurons misfire or degenerate, the NYSCF team creates “disease in a dish” models by reprogramming patients’ skin and or blood samples into induced pluripotent stem (iPS) cells that can become neurons and the other brain cells affected in the diseases.

The cells in our body form three-dimensional networks, essential to tissue function and overall health; however, previous techniques to form complex brain tissue resulted in structures that, while similar in form to naturally occurring neurons, undermined imaging or electrical recording attempts.

In the current study, the Noggle and Nestor with NYSCF scientists specially adapted two-dimensional culture methods to grow three-dimensional neuron structures from iPS cells. The resultant neurons were “thinned-out,” enabling calcium-imaging studies, which measure the electrical activity of cells like neurons.

“Combining the advantages of iPS cells grown in a 3D environment with those of a 2D system, our technique produces cells that can be used to observe electrical activity of putative networks of biologically active neurons, while simultaneously imaging them,” said Nestor. “This is key to modeling and studying neurodegenerative diseases.”

Neural networks, thought to underlie learning and memory, become disrupted in Alzheimer’s disease. By generating aggregates from iPS cells and comparing these to an actual patient’s brain tissue, scientists may uncover how disease interferes with these cell-to-cell interactions and understand how to intervene to slow or stop Alzheimer’s disease.

“This critical new tool developed by our Alzheimer’s team will accelerate Alzheimer’s research, enabling more accurate manipulation of cells to find a cure to this disease,” said Susan L. Solomon, CEO of NYSCF.

Reblogged from Neuromorphogenesis!

What Is Alzheimer’s Disease ?

(via amadeus9019)

Reblogged from Elias. T