Mice with disorders similar to Alzheimer’s, perceived a familiar setting, like new, and the activity of neurons from the novelty of them drowns out the commemorative track. The researchers suppressed the activity of neurons in novelty, and the animals remembered a forgotten the context. When healthy animals activated the “noise” of a neural network, they were unable to recall the situation. The results, published in the journal Nature Neuroscience, reveal a new direction in the research of dementia and its treatment
When we memorize new information, the brain forms a memorable trace, or engram, neural recording in the brain. In recall neurons engrams are activated, and the suppression of their work leads to forgetting.
Memory impairment is the main manifestation of dementia, the most common form of which is Alzheimer’s disease. Memory impairment in this disease is associated with damage to area CA1 of the hippocampus — it is necessary for the formation and retrieval of memory and plays the role of indicator of new developments. Neurons from area CA1 of mouse models of Alzheimer’s disease hyperactive in the area of amyloid plaques (an important marker of the disease), perhaps this leads to a violation of engrams.
Scientists from Germany under the leadership of Martin Furmanny (Martin Fuhrmann) from the German center for neurodegenerative diseases engram investigated context-dependent memory in area CA1 of the hippocampus of mice with disorders similar to Alzheimer’s disease. This followed the expression of the immediate early gene c-fos , it is connected with the activity of neurons and are convenient for marking memorable tracks. Transgenic mice neurons simultaneously with c-fos was allocated a green fluorescent protein – with the brightness of its light in freely moving animals the researchers observed through the glass window in the skull using two-photon microscope.
The expression of c-fos in the same neurons was observed during the three phases of the experiment. For a start, researchers recorded a baseline level of neuronal activity. Then the mice were trained fear response to a specific context: the animals were placed in an experimental chamber, were given her to examine, and then electrocuted. After two days spent testing: mice were placed in either the same camera or another one and check if they remember the context of threat and fear him.
Basic level expression of c-fos in mice with model of Alzheimer’s disease and control did not differ (although in the area of amyloid plaques, the neurons were more active). Researchers have identified two populations of nerve cells: neurons, the expression of c-fos which remained at the same level and those are then amplified, then reduced their activity.
In the new cell mice from both groups actively explored the environment, and the number of activated neurons in area CA1 have them matched. However, when testing mouse model of Alzheimer’s disease is not afraid of the camera, which was recently electrocuted, and the expression of c-fos in the hippocampus was the same as during the examination of the new situation. In other words, the mouse did not remember associated with the context of an unpleasant experience. Control animals were frozen (so mouse show fear) in the “threat” to the camera, and the new neurons were not activated.