The researchers concentrated on two areas of the brain, the hippocampus and the frontal cortex, areas where plaque formation occurs in humans.
Researchers at Stanford University and MIT's Picower Institute for Learning and Memory had activated light-sensitive neurons in the brain's hippocampus involved in the memory of fright.
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Dr. James Stone, who authored the research, says that the signaling between these two types of neurotransmitter is happening between a part of the brain called the hippocampus and another called the striatum.
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Oligomers, which are considered more toxic to brain tissue than amyloid-beta proteins, were applied to the hippocampus, the brain's memory center, in young mice.
Imaging studies on depressed humans show shrinkage in their hippocampus, a brain region involved in learning, memory and emotion that is also a region where much neurogenesis occurs.
The jet-lagged hamsters showed a drastic drop in neuron production in the hippocampus area of the brain, which closely contributes to memory processing and learning.
With time, neuroscience research uncovered two parts of the brain that evidence neurogenesis: the hippocampus, associated with memory formation, and the olfactory bulb, associated with the sense of smell.
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Scans also show that the temporal lobe, which contains the hippocampus, and another brain region called the posterior cingulate use less glucose than a normal brain, suggesting they have shut down.
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The data was then processed and showed people with schizophrenia had fewer successful "dockings" in the left hippocampus area in the brain - an area known to be involved in learning, perception and memory - than healthy people.
This work shows that sleep trains the brain and promotes memory reorganisation from the hippocampus to the striatum, meaning that navigation becomes more automatic.
But scientific studies have taken things one step further and shown that as cab drivers hone their skills, their hippocampus -- the part of the brain that deals with spatial memory and navigation -- gradually gets bigger.
This is done by examining the combined concentration of gray and white matter, or nerve cells and fiber tracts, in parts of the brain not normally used for verbal processing the hippocampus and cerebellum, normally associated with memory and motor learning.
The hippocampus is an area at the base of the brain in humans, close to the junction with the spinal cord.
Eugenol, like other antidepressants, increases expression of brain-derived neurotrophic factor (BDNF) gene in the hippocampus, which is necessary for an antidepressant to exhibit its activity.
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The limbic system, in particular the amygdala (an almond shaped region that is located just in front of the hippocampus), is the first part of the brain to receive emotional information and react to it.
The hippocampus, for example, is a part of the brain in the medial temporal lobe, which is very active in spatial navigation and memory.
These grid cells create a direct, intuitively simple map of everywhere you go, basically, sending the data to your hippocampus, the seat of memory and emotion in your brain.
They concentrate on the hippocampus -- part of the cerebral cortex which sits deep in the brain -- where short-term memories become long-term ones.
One question: Why would regrowth in the hippocampus reverse depression, when the ailment also affects many other areas of the brain?
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