Memory Loss Caused by Brain Damage Is Reversible, Says Study

Degenerative brain diseases, including Alzheimer’s, could one day be treated with drugs that can reverse distressing loss of memory, according to a study released this week.

The very term “memory loss” could be a misnomer in such cases, suggests the study, published in British journal Nature: that cherished recollection of a first kiss, seemingly destroyed by disease, may have simply been rendered inaccessible by obstructed neural pathways.

In laboratory experiments, mice suffering the type of brain damage that in humans typically leads to dementia – robbing victims of the ability to remember past events or even to recognize loved ones – were able to recover memories acquired during earlier conditioning, according to the study carried out by researchers at the Massachusetts Institute of Technology.

Following a period of rehabilitation through mental stimulation, the genetically modified mice successfully performed tasks they had “forgotten” in the wake of damage inflicted on specific neural networks in the brain.

The same regenerative results were also later obtained through a drug treatment.

While there is no guarantee that the same techniques will work in humans, the study does raise “the possibility of recovering long-term memories in patients” ravaged by certain neurological disorders, according to lead author Li-Huei Tsai, who conducted the study with four colleagues.

Neurodegenerative diseases attack those parts of the brain and spinal cord that control bodily movement and process information stored in the form of memories.

When brain cells deteriorate or are destroyed, they are not replaced. Earlier studies have shown, however, that healthy neurons stimulated through mental activity or directly by chemicals can grow stronger and reconfigure themselves.

Tsai’s breakthrough in a series of ingenious experiments was to demonstrate that this same process of remodeling can be reparative, unlocking memories rendered inaccessible by diseases causing “significant brain atrophy and neuronal loss.”

The researchers began their experiment by selecting genetically modified mice in which a protein linked to neurodegenerative disease, called p25, could be switched “on” or “off” chemically.

Before this brain-damaging protein was activated, the mice demonstrated in two tests that they had learned how to avoid an electric shock, and how to navigate a maze quickly for a food reward.

After the animals were subjected to six weeks of neurological degeneration, they could no longer perform these tasks. But an intensive, four-week regimen of “environmental enrichment” – scientific jargon for access to lots of toys and play – led to a sharp increase in learning ability and memory. Indeed, the mice passed the tests almost as well as control mice.

The researchers were careful to focus on long-term memories, thought to be stored in the cortical network, and not recently learned behavior, which is initially encoded in another part of the brain, the hippocampus.

Tsai and her colleagues had a hunch as to what was going on at a molecular level when the memories were retrieved and devised a further experiment to test it by chemically inhibiting an enzyme – histone deacetylase (HDAC) – known to interfere with gene transcription.

The results showed the same beneficial effect as the “environmental enhancement,” suggesting that it could be the basis for a pharmaceutical treatment for memory loss.

“Using small molecules that target HDACs in patients with dementia could facilitate access to long-terms memories,” the study concludes.

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