Memory loss in Alzheimer’s disease is linked to “replay mode” problems in the brain, researchers say.
According to IsnaTo consolidate memories, our brain replays them during rest periods as a kind of “replay mode”. A new study on mice shows that disruption of this process can play a role in the memory loss that is one of the complications of Alzheimer’s disease.
According to the University College London research team, the findings could pave the way for opportunities to diagnose Alzheimer’s at an early stage and treat the associated brain damage.
Neuroscieist Sarah Shipley says Alzheimer’s disease is caused by the accumulation of harmful proteins and plaques in the brain, leading to symptoms such as memory loss and disorieation, but it is not clear exactly how these plaques disrupt normal brain processes.
He added: “We waed to understand how the function of brain cells changes as the disease progresses to determine what causes these symptoms.”
The studied mice were put in conditions similar to Alzheimer’s with the toxic accumulation of “amyloid beta” protein in their brains. These experimeal animals showed signs of being unable to register a spatial map in their memory while navigating the spirals.
Both during the spiral challenges and while the rats were resting between sessions, Shipley and his colleagues monitored the activity of their hippocampus, an area of the brain that coains spatial memory neurons known as place cells.
In order for the mice to remember where they have been, these cells must be activated in a specific order. As memories are “stored” for long-term storage, that activation sequence repeats itself like a replay.
The frequency of these repeats did not change in mice with amyloid-beta plaques in their brains, but the order of the sequences did. It was as if the memories were scenes from a short film that had been cut io pieces and stored in differe places.
This was also observed in spiral navigation behavior, with lesioned rats often forgetting which parts of the spiral they had previously visited (even within a single session). Place cells also became more unstable over time, and cell-to-place mapping was disrupted.
Although this study used a model of Alzheimer’s in the brain of mice, there are good reasons to believe that the same type of impairme occurs in humans with the disease, something that could be confirmed through future studies.
Neuroscieist Caswell Barry says: We have discovered a disorder in the way the brain consolidates memories, which is visible at the level of individual neurons. Notably, replay eves still occur, but have lost their natural structure. It’s not that the brain stops trying to consolidate memories, but that the process itself is impaired.
Alzheimer’s disease is a complex disease with multiple risk factors. There are many differe poteial causes and couless influences on the brain that may work together or separately.
Part of the difficulty for researchers is trying to figure out what causes Alzheimer’s to develop and what happens as a result, and that uncertaiy is also prese in the build-up of amyloid beta.
Studies like this add pieces to the overall puzzle, allowing us to see more of the “big picture of Alzheimer’s” and how all these causes and effects fit together as brain function declines over time.
Each new discovery means we may be able to detect symptoms earlier, allowing more time for treatmes and supports, and developing treatmes to target specific parts of Alzheimer’s.
In this case, the result may be the developme of drugs that help iensify the feedforward activity in hippocampal place cells. However, this will not be possible uil further research can ideify the processes involved and how to specifically regulate them safely.
“We hope our findings can help develop tests to diagnose Alzheimer’s early, before extensive damage has occurred, or lead to new treatmes that target this relapsing process,” says Berry.
This research was published in Curre Biology magazine.
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