Destructive plaques found in the brains of Alzheimer’s patients have been rapidly cleared by researchers testing a cancer drug on mice. The US study, published in the journal Science, reported the plaques were broken down at “unprecedented” speed.
Posts tagged biology.
“Australian scientists sequenced the DNA of samples of the giant seagrass, Posidonia oceanic, from 40 underwater meadows in an area spanning more than 2,000 miles, from Spain to Cyprus.
The analysis, published in the journal PLos ONE, found the seagrass was between 12,000 and 200,000 years old and was most likely to be at least 100,000 years old. This is far older than the current known oldest species, a Tasmanian plant that is believed to be 43,000 years old. […]”
“Alzheimer’s disease seems to spread like an infection from brain cell to brain cell, two new studies in mice have found. But instead of viruses or bacteria, what is being spread is a distorted protein known as tau.
The surprising finding answers a longstanding question and has immediate implications for developing treatments, researchers said. And they suspect that other degenerative brain diseases like Parkinson’s may spread in a similar way.”
A donor heart beating in a mechanical system which keeps it warm, oxygenated, with nutrient enriched blood pumping through.
12 December 1980: John Lorber, a British neurologist, claims that some patients are more normal than would be inferred from their brain scans.
“Professor John Lorber has a facility for making doctors sit up and think about hallowed concepts,” writes Adrian Bower, a neuroanatomist at Sheffield University, England, where Lorber holds a research chair in pediatrics. “The human brain is the current object of his challenging speculation,” continues Bower, referring to his colleague’s recent propositions concerning hydrocephalus, or water on the brain. For instance, Lorber was not jesting totally when he addressed a conference of pediatricians with a paper entitled “Is your brain really necessary?” Lorber believes that his observations on a series of hydrocephalics who have severely reduced brain tissue throws into question many traditional notions about the brain, both in clinical and scientific terms.
Memories in our brains are maintained by connections between neurons called “synapses.” But how do these synapses stay strong and keep memories alive for decades? Neuroscientists at the Stowers Institute for Medical Research have discovered a major clue from a study in fruit flies: Hardy, self-copying clusters or oligomers of a synapse protein are an essential ingredient for the formation of long-term memory.
The finding supports a surprising new theory about memory, and may have a profound impact on explaining other oligomer-linked functions and diseases in the brain, including Alzheimer’s disease and prion diseases.
“Self-sustaining populations of oligomers located at synapses may be the key to the long-term synaptic changes that underlie memory; in fact, our finding hints that oligomers play a wider role in the brain than has been thought,” says Kausik Si, Ph.D., an associate investigator at the Stowers Institute, and senior author of the new study, which is published in the January 27, 2012 online issue of the journal Cell.
Si’s investigations in this area began nearly a decade ago during his doctoral research in the Columbia University laboratory of Nobel-winning neuroscientist Eric Kandel. He found that in the sea slug Aplysia californica, which has long been favored by neuroscientists for memory experiments because of its large, easily-studied neurons, a synapse-maintenance protein known as CPEB (Cytoplasmic Polyadenylation Element Binding protein) has an unexpected property.
A portion of the structure is self-complementary and — much like empty egg cartons — can easily stack up with other copies of itself. CPEB thus exists in neurons partly in the form of oligomers, which increase in number when neuronal synapses strengthen. These oligomers have a hardy resistance to ordinary solvents, and within neurons may be much more stable than single-copy “monomers” of CPEB. They also seem to actively sustain their population by serving as templates for the formation of new oligomers from free monomers in the vicinity.
CPEB-like proteins exist in all animals, and in brain cells they play a key role in maintaining the production of other synapse-strengthening proteins. Studies by Si and others in the past few years have hinted that CPEB’s tendency to oligomerize is not merely incidental, but is indeed essential to its ability to stabilize longer-term memory. “What we’ve lacked till now are experiments showing this conclusively,” Si says.
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The tip of a girl’s 40,000-year-old pinky finger found in a cold Siberian cave, paired with faster and cheaper genetic sequencing technology, is helping scientists draw a surprisingly complex new picture of human origins.
The new view is fast supplanting the traditional idea that modern humans triumphantly marched out of Africa about 50,000 years ago, replacing all other types that had gone before. Instead, the genetic analysis shows, modern humans encountered and bred with at least two groups of ancient humans in relatively recent times: the Neanderthals, who lived in Europe and Asia, dying out roughly 30,000 years ago, and a mysterious group known as the Denisovans, who lived in Asia and most likely vanished around the same time.
Neanderthals Had Differently Organised Brains
Homo neanderthalensis is not a species to be dismissed lightly. They weren’t especially dumb, nor especially weak. Indeed, they actually had larger brains and denser muscles than we did.
On top of that, their technology was so well adapted to their environment that they were able to flourish without drastically altering it for hundreds of thousands of years. It was just that good.
So it would seem we have no clear advantage over them, which makes the fact we survived but they did not especially puzzling.
Recent research argues this might have been because their brain, despite being bigger, ultimately had a more primitive shape. Our frontal and temporal lobes are a different to theirs and our olfactory bulb is larger. Could our brain shape have given us an advantage?
Now, new information presented at the HOBET conference I recently attended lends further credibility to that hypothesis.
“A new study of women ages 18 to 44 found that drinking coffee and other caffeinated beverages can alter levels of estrogen. But the impact varies by race. In white women, for example, coffee appears to lower estrogen, while in Asian women it has the reverse effect, raising levels of the hormone.”
A healthy human brain (left) compared to the brain of a 90 year old (right) which is only two thirds the size of the young brain. Over time, white matter decreases and the brain shrinks. This gradual shrinkage is most extreme between age 70 and 80.
Aging mice can be made “young” again, according to findings one scientist initially found unbelievable. The key is muscle-derived stem cells, which—like other stem cells—are unspecialized cells that can become any type of cell in the body. When injected with muscle stem cells from young mice, older mice with a condition that causes them to age rapidly saw a threefold increase in their life spans, said study co-author Johnny Huard, a stem-cell expert at the McGowan Institute for Regenerative Medicine in Pittsburgh.
Everyone has seen at least one episode of a medical mystery series. The doctors, having no real idea what the patient could be suffering from, are forced to treat patients based on hunches. Wouldn’t it just be so much easier if we could look through their DNA to see if there’s some form of weird code leading to an obscure disease, outlining their symptoms perfectly?
That’s actually not very far from the truth now. After the success of the Human Genome Project, many new mysteries have been solved and advancements have been made, the most recent of which being the diagnosis of patients with hard-to-pinpoint metabolic diseases being applied to the hospitals themselves.
This is particularly useful in mitochondrial diseases as these, according to New Scientist, ”are notoriously difficult to diagnose. …the diseases often involve many genes, and symptoms vary across organs. Currently, diagnosing such disorders can take months or even years, and involves an invasive muscle biopsy. DNA sequencing technology may help to speed things up.”