Treating astrocytes can help eliminate plaquer in Alzheimer's disease

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Medical News Today


When brain cells start oozing too much of the amyloid protein that is the hallmark of Alzheimer's disease, the astrocytes that normally nourish and protect them deliver a suicide package instead, researchers report.


Amyloid is excreted by all neurons, but rates increase with aging and dramatically accelerate in Alzheimer's. Astrocytes, which deliver blood, oxygen and nutrients to neurons in addition to hauling off some of their garbage, get activated and inflamed by excessive amyloid.


Now researchers have shown another way astrocytes respond is by packaging the lipid ceramide with the protein PAR-4, which independently can do damage but together are a more "deadly duo," said Dr. Erhard Bieberich, biochemist at the Medical College of Georgia at Georgia Health Sciences University.


"If the neuron makes something toxic and dumps it at your door, what would you do?" said Bieberich, corresponding author of the study published in the Journal of Biological Chemistry. "You would probably do something to defend yourself."


The researchers hypothesize that this lipid-coated package ultimately kills them both, which could help explain the brain-cell death and shrinkage that occurs in Alzheimer's. "If the astrocytes die, the neurons die," Bieberich said, noting studies suggest that excess amyloid alone does not kill brain cells. "There must be a secondary process toxifying the amyloid; otherwise the neuron would self-intoxicate before it made a big plaque," he said. "The neuron would die first."


One of many avenues for future pursuit include whether a ceramide antibody could be a viable Alzheimer's treatment. In the researchers' studies of brain cells of humans with Alzheimer's as well as an animal model of the disease, antibodies to ceramide and Par-4 prevented astrocytes' amyloid-induced death.
apoxosomes
Ceramide and Par-4 get packaged in lipid-coated vesicles called exosomes; all cells secrete housands of these vesicles but scientists are only beginning to understand their normal function. When exosomes become deadly, they are called apoxosomes.


Ceramide and Par-4 are typically not in a vesicle, rather in two distinct parts of a cell. Ceramide appears to take the lead in bringing the two together when confronted with amyloid. Bieberich and colleagues at the University of Georgia reported in 2003 that the deadly duo helps eliminate duplicate brain cells that occur early in brain development when their survival could result in a malformed brain. They suspected then that the duo might also have a role in Alzheimer's.


Risk factors for Alzheimer's include aging, family history and genetics, according to the Alzheimer's Association. Increasing evidence suggests that Alzheimer's also shares many of the same risk factors for cardiovascular disease, such as high cholesterol, high blood pressure and inactivity.

Hope for dementia patients after Alzheimer's cells created in lab for first time Read more: http://www.dailymail.co.uk/health/article-2091716/Hope-dementia-patients-Alzheimers-cells-created-lab-time.html#ixzz1kWG64NIL

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

Mail Online

Cells damaged by Alzheimer's created for first time
Hoped discovery will enable better understanding of dementia

By SADIE WHITELOCKS

Brain cells damaged by Alzheimer's have been created for the first time, offering hope to dementia patients.
It is believe that the breakthrough could help scientists better understand how the degenerative condition affects the the nervous system, prompting more effective treatment.
Alzheimer's is characterised by loss of neurons and synapses, leading to gradual memory loss and difficulties with language and emotions.

And until now investigations have been limited to 'non-neuronal human cells' or 'animal models'.
However a team from the University of California have developed a way of growing human cells.
Currently there is no cure for Alzheimer’s disease, but medication is available that can slow down its development.

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During the research skin cells from two patients with a rare inherited form of Alzheimer's were taken and used to create neurons displaying biochemical hallmarks of the disease.
Lead researcher Professor Lawrence Goldstein, said: 'Creating highly purified and functional human Alzheimer's neurons in a dish - this has never been done before.
'It's a first step. These aren't perfect models. They're proof of concept. But now we know how to make them.
'It requires extraordinary care and diligence, really rigorous quality controls to induce consistent behaviour, but we can do it.'
Professsor Goldstein highlighted in the paper, published in the journal Nature, that differences between a healthy neuron and an Alzheimer's neuron are subtle.
But being able to grow Alzheimer's neurons will help scientists to better understand how the nervous system is impacted and which drugs would be most effective.
He added: 'We need to do everything we can because the cost of this disease is just too heavy and horrible to contemplate.
'Without solutions, it will bankrupt us - emotionally and financially.'
Further research is now underway.
He said: 'We're dealing with the human brain. You can't just do a biopsy on living patients.
'Instead, researchers have had to work around, mimicking some aspects of the disease in . Neither approach is really satisfactory.'
Alzheimer's disease is the most common form of dementia, which is a group of symptoms associated with a decline in mental abilities, such as memory and reasoning and is most common in people aged over 65.
It attacks nerves, brain cells and neurotransmitters (chemicals that carry messages to and from the brain).
Dementia affects around 5.4 million people in the US, with Alzheimer’s disease responsible for around 60 per cent of all cases.