M.I.T. Lab Restores lost memories in Alzheimer ;
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In Alzheimer’s disease patients are often unable to remember recent experiences. A new M.I.T. Study in mice suggests that these memories are stored in the brain – that simply can not be easily accessed. This raises the possibility of investing some memory loss in the early stages of Alzheimer’s disease. Learn how.
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Moreover, the researchers were able to artificially stimulate those memories using a technique known as optogenetics, suggesting that these memories can still be recovered with a little help.
Although optogenetic not be currently used in humans, the results raise the possibility of developing future treatments that could reverse some of the memory loss is seen in the early stages of Alzheimer’s disease, say researchers.
“the important point is that this is a proof of concept, that is, even if a memory seems to have disappeared, it is still there. it’s a question of how to recover “said Susumu Tonegawa, professor Picower of Biology and Neuroscience and director of the RIKEN-MIT Center for Neural Circuit Genetics Picower Institute for Learning and Memory.
Tonegawa is the lead author of the study, published in the March 16 online edition of Nature . Dheeraj Roy, a graduate student at MIT, is the lead author of the article.
In recent years, Tonegawa laboratory identified cells in the hippocampus of the brain that store specific memories. Researchers have also shown that they can manipulate these memory traces or engrams, to plant false memories, activate existing memories, or alter the emotional associations of a memory.
Last year, Tonegawa, Roy, and his colleagues found that mice with retrograde amnesia following a traumatic injury or stress, had impaired memory retrieval, but could still form new memories . That led the team to wonder whether this might also be true for the memory loss seen in the early stages of Alzheimer’s disease, previously characteristic amyloid plaques appear in the brains of patients occurs.
To investigate this possibility, the researchers studied two different strains of mice genetically engineered to develop Alzheimer’s symptoms, and a group of healthy mice.
All these mice, when exposed to a chamber where they received a footshock showed fear when placed in the same chamber an hour later. However, when placed in the camera again several days later, only normal mice still showed fear. Alzheimer’s mice did not seem to remember the foot shock.
“The short-term memory seems to be normal, the order of hours. However, for long-term memory, the mice of these early Alzheimer seem to be impaired,” says Roy.
the researchers then showed that while mice can not remember their experiences when prompted by natural signs, those memories are still there.
To demonstrate this, first engrams tagged cells associated with the terrible experience with a light-sensitive protein called channelrhodopsin, using a technique developed in 2012. Each time these engrams labeled cells are activated by light, normal mice remember encoded by that group of memory cells. Similarly, when the researchers placed mice in a chamber Alzheimer had never seen before and shone the light in the cells of engrams encoding fearful experience, the mice showed fear immediately.
“directly activating cells that we believe are holding memory gets them to recover,” says Roy. “This suggests that it is a problem of access to information, is not that they are unable to learn or store this memory.”
The researchers also showed that cells from mice of Alzheimer engrams had fewer dendritic spines, which are small buds that allow neurons receive input signals from other neurons.
Normally, when a new memory is generated, the cells corresponding to that memory engrams grow new dendritic spines, but this did not happen in the Alzheimer mice. This suggests that cells engrams are not receiving sensory information from another part of the brain called the entorhinal cortex. The natural signal that should revive the memory – being in the camera again – has no effect because the sensory information does not enter cells engrams
“If we want to recall a memory, the memory retaining the. cells have to be reactivated by the correct signal. If the density of the spine does not rise during the learning process, and later, if given a signal natural reminder, you may not be able to reach the cell nucleus engrams, “said Tonegawa.
“This is a remarkable study provides the first proof that the deficit earliest Alzheimer’s disease memory involves the recovery of the consolidated information,” says Rudolph Tanzi, a neurology professor at the Faculty of Medicine Harvard, who was not involved in the research. “As a result, the implications for the treatment of memory deficits of Alzheimer’s disease based on the strengthening of synapses are extremely exciting.”
the researchers were also able to induce a long-term revival of the “lost” memories by stimulating new connections between the entorhinal cortex and hippocampus.
To achieve this, light is used to stimulate optogenetically cells of the entorhinal cortex that feed into the hippocampal cells engrams encoding the fearful memory. After three hours of this treatment, the researchers expected a week and the mice were tested again. This time, the mice could recover the memory on their own when placed in the original camera, and were much more dendritic spines in their cells engrams.
However, this approach does not work if a very large section of the entorhinal cortex is stimulated, suggesting that any potential treatment for human patients would have to be very specific. Optogenetics is very accurate but too invasive for use in humans, and existing methods for deep brain stimulation – a form of electrical stimulation sometimes used to treat Parkinson’s and other diseases -. Too affect the brain
“It is possible that future technology to activate or inactivate the cells inside the brain such as the hippocampus and the entorhinal cortex, more precisely be developed,” said Tonegawa. “The basic research conducted in this study provides information on the populations of targeted cells, which is critical for treatment and future technologies.”
This article was originally published on alzheimersweekly, Read the original article here