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New Hope to Alzheimer’s Disease Therapy

Alzheimer’s disease is the most common form of dementia that affects over five million Americans each year. It is a memory loss that occurs due to age or other diseases. About 60 to 80% of people living with dementia are believed to have Alzheimer.

The main impact of Alzheimer’s disease is memory loss – but memory loss does not always mean Alzheimer. There are many other factors such as trauma that can be responsible for memory loss. However, once Alzheimer’s starts developing, memories start to decline in episodes. That is, memories of personal experiences – events, time, place and emotional state – start to fade. According to the Mayo Clinic, “In Alzheimer’s disease, the brain cells degenerate and die, causing a steady decline in memory and mental function,” and this development usually starts occurring around age 60. The more an individual age, the more at risk they are to develop the disease.

Other symptoms of Alzheimer’s disease include: Change in behavior, Wandering, Impaired reasoning, Motor Dysfunctions, among others; and it is important to note that there is presently no cure for Alzheimer’s disease.

For a memory to be recalled, four things must be available:

  • The ability to encode
  • The resource to consolidate
  • Be able to store and
  • The ability to retrieve information.

When one of these processes gets compromised, memories become inaccessible, since they were never encoded (a message was never formed), stored, the memories are unable to be accessed by the individual.

However, the challenging part of the study of Alzheimer’s disease is finding out what part of the memory is disrupted in an Alzheimer’s patient. Usually, recent memories are the first to be forgotten, therefore, the ability to save new information is the most compromised aspect of memory mechanisms in Alzheimer’s patients – at least in its early stages.

Although some studies support this hypothesis, it is not an easy thing to determine beyond doubt with currently available tools. Therefore, the question, “How can we be sure if a memory was not stored, or if it is just inaccessible?”, has been hatched repeatedly. Therefore, bypassing the process of memory recall to check if a memory is stored is not an easy fit.

Recent studies in animals have, however, provided great insights into the neurological mechanisms of memory loss in Alzheimer’s disease. A recently published study in Nature throws more light into the mechanisms of memory loss associated with Alzheimer’s and brings a light at the end of the tunnel type of possibility that lost memories may be recoverable.

The main purpose of the research was to find out if memories are absent, or just unreachable. The group of researchers from the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory set about their research using a mouse model of Alzheimer’s disease.

They designed a simple yet enlightening experiment:

Two groups of mice were genetically engineered to develop Alzheimer’s symptoms – one with early-stage Alzheimer’s, the other with an advanced version of the disease. The third group consisted of healthy mice.

When placed in the same chamber after an hour of the initial foot shock, both the healthy and early-stage Alzheimer’s mice displayed fear. Meaning both could still recall the earlier shock to the foot; whereas the advanced-stage Alzheimer’s mice did not display fear. This shows that those with early-stage symptoms could still encode and store memories on a short-term time frame unlike those with advanced-stage Alzheimer.

However, 24 hours after the initial shock, in the same chamber, only the healthy mice showed signs of fear. Mice with Alzheimer’s symptoms showed no sign of remembering the foot shock, which suggests that, though new memory had been stored, the mice were now unable to retrieve the memory. It was more like they were in the chamber for the first time and had no reason to be afraid in there.

The researchers went further to study the possibility of retrieving those memories in mice with early-stage Alzheimer’s.

First, they used molecular, genetic and optogenetic methods to pinpoint the neuronal cells with traces (engrams) of the fearful memory of the foot shock, and tagged them with a light-sensitive molecule. Then, using blue light, they stimulated those cells in the hippocampus responsible for memory recall – the memory engram cells. This method had already been seen to work for memory retrieval in other forms of memory loss.

The research showed blue-light stimulation can indeed bring back the memory of the foot shock. Direct activation of the cells holding the memory allowed the memory to be retrieved as effectively as in the healthy mice.

The study also showed that the neurons holding the memory have structural changes that affect their signals to the other cells. The changes tampered with their ability to receive sensory signals from other cells, which act as a cue for memory recall. Meaning, although the memory was stored, when the mice were placed in the chamber where the foot shock took place, the sight of the chamber did not trigger the fearful memory as it should have. The blue-light stimulation serves as a substitute for that sensory trigger of memory.

From this study, it can be said that new memories are most likely still being formed in the early stages of Alzheimer disease in humans, but their retrieval process might be compromised.

It is pertinent to note that this memory loss may be overcome using brain stimulation; and although present technology is still incapable of carrying out the necessary process on humans, the study brings new optimism, new hope to Alzheimer’s disease therapy.

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