Lost memories might be able to be restored, new UCLA study indicates

via modernevil.com

via modernevil.com

New UCLA research indicates that lost memories can be restored. The findings offer some hope for patients in the early stages of Alzheimer’s disease.

For decades, most neuroscientists have believed that memories are stored at the synapses — the connections between brain cells, or neurons — which are destroyed by Alzheimer’s disease. The new study provides evidence contradicting the idea that long-term memory is stored at synapses.

“Long-term memory is not stored at the synapse,” said David Glanzman, a senior author of the study, and a UCLA professor of integrative biology and physiology and of neurobiology. “That’s a radical idea, but that’s where the evidence leads. The nervous system appears to be able to regenerate lost synaptic connections. If you can restore the synaptic connections, the memory will come back. It won’t be easy, but I believe it’s possible.”

The findings were published recently in eLife, a highly regarded open-access online science journal.

Glanzman’s research team studies a type of marine snail called Aplysia to understand the animal’s learning and memory. The Aplysia displays a defensive response to protect its gill from potential harm, and the researchers are especially interested in its withdrawal reflex and the sensory and motor neurons that produce it.

They enhanced the snail’s withdrawal reflex by giving it several mild electrical shocks on its tail. The enhancement lasts for days after a series of electrical shocks, which indicates the snail’s long-term memory. Glanzman explained that the shock causes the hormone serotonin to be released in the snail’s central nervous system.

Long-term memory is a function of the growth of new synaptic connections caused by the serotonin, said Glanzman, a member of UCLA’s Brain Research Institute. As long-term memories are formed, the brain creates new proteins that are involved in making new synapses. If that process is disrupted — for example by a concussion or other injury — the proteins may not be synthesized and long-term memories cannot form.  (This is why people cannot remember what happened moments before a concussion.)

“If you train an animal on a task, inhibit its ability to produce proteins immediately after training, and then test it 24 hours later, the animal doesn’t remember the training,” Glanzman said.  “However, if you train an animal, wait 24 hours, and then inject a protein synthesis inhibitor in its brain, the animal shows perfectly good memory 24 hours later.  In other words, once memories are formed, if you temporarily disrupt protein synthesis, it doesn’t affect long-term memory. That’s true in the Aplysia and in human’s brains.”  (This explains why people’s older memories typically survive following a concussion.)

Glanzman’s team found the same mechanism held true when studying the snail’s neurons in a Petri dish. The researchers placed the sensory and motor neurons that mediate the snail’s withdrawal reflex in a Petri dish, where the neurons re-formed the synaptic connections that existed when the neurons were inside the snail’s body.  When serotonin was added to the dish, new synaptic connections formed between the sensory and motor neurons.  But if the addition of serotonin was immediately followed by the addition of a substance that inhibits protein synthesis, the new synaptic growth was blocked; long-term memory could not be formed.

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Barrier breaking drug may lead to spinal cord injury treatments

Scientists developed a drug that allows axons to cross impenetrable barriers leading to the treatment of spinal cord injuries. Courtesy of Silver lab, Case Western Reserve School of Medicine

Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health.

The results demonstrate how fundamental laboratory research may lead to new therapies.

“We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature.

Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury.

On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require.

NIH-funded scientists developed a promising new drug that may lead to spinal cord injury treatments.Video courtesy of the NINDS and Silver lab, Case Western Reserve School of Medicine.

“Originally this was just a side project we brainstormed in the lab,” said Dr. Lang.

After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.

Dr. Lang and his colleagues designed a drug called ISP to block the enzyme and facilitate the drug’s entry into the brain and spinal cord. Injections of the drug under the skin of paralyzed rats near the injury site partially restored axon growth and improved movements and bladder functions.

“There are currently no drug therapies available that improve the very limited natural recovery from spinal cord injuries that patients experience,” said Lyn Jakeman, Ph.D., a program director at the NIH’s National Institute of Neurological Disorders and Stroke, Bethesda, MD. “This is a great step towards identifying a novel agent for helping people recover.”

Initially, the goal of the study was to understand how interactions between PTP sigma and chondroitin sulfate proteoglycans prevent axon growth. Drugs were designed to mimic the shape of a critical part of PTP sigma, called the wedge. Different designs were tested on neurons grown in petri dishes alongside impenetrable barriers of proteoglycans. Treatment with ISP freed axon growth.

“It was amazing. The axons kept growing and growing,” said Dr. Silver.

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