Scientists may have found a way to restore memory in dementia patients

As the researchers receive $10 million in federal funding to carry out trials of a breakthrough ultrasound technique on humans, the possibility of memory being restored among dementia patients may become a reality soon.

Researchers had recently tested the technology in animal models to remove toxic amyloid-beta plaques from the brain. It helped them successfully reverse Alzheimer's symptoms and restore memory function in the animal model. It involves injecting “micro bubbles” in the brains of mice which, when used with an ultrasound, fully restored their brain function.

The grant will help the researchers test the method on up to 10 patients with early-onset dementia. A Prof. told the media that researchers had shown the approach worked in sheep and mice, and the next step was to go into human participants and start with the "safety trial".

The next stage will be developing the technology into a portable scanning device. According to the World Health Organization, by 2050, there will be more than three-fold increase in the number of people suffering from dementia from 50 million to 152 million.

In the backdrop of this data, the study and upcoming trials raise hopes for millions around the world.

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Alzheimer's news: More than a hundred key 'memory' genes identified by researchers

It means drugs being developed to combat the devastating neurological illness could be given to patients sooner - even decades before symptoms develop.

Researcher has shown the greatest fear for people is they may end their days slipping into dementia - even ahead of suffering heart disease or cancer.

A new study is the first to find links between genes and brain activity during memory processing - providing a new window into memory.

Dr Genevieve Konopka of University of Texas Southwestern said: "This is very exciting because the identification of these gene-to-behaviour relationships opens up new research avenues for testing the role of these genes in specific aspects of memory function and dysfunction.

"It means we are closer to understanding the molecular mechanisms supporting human memory and thus will be able to use this information someday to assist with all kinds of memory issues."

Her findings presented to a Cognitive Neuroscience Society conference in San Francisco is part of the emerging field of 'imaging genetics' which investigates mutations in the function and anatomy of the brain.

A pill to combat dementia is predicted to be available within a decade.

Only in December a widely anticipated drug called solanezumab failed.

But experts believe this was because it was given to people with early Alzheimer's which even then may have been too late because irreversible brain damage had already occurred.

Identifying patients likely to develop memory problems would in future allow medications to be prescribed even sooner.

While past work has aimed to connect behaviour to genes researchers have lacked neural markers - which can provide a powerful bridge between the two.

Dr Evelina Fedorenko, of Harvard Medical School in Boston, who is chairing the symposium on imaging genetics, said: "Genes shape the anatomy and functional organisation of the brain and these structural and functional characteristics give rise to the observable behaviours."

The field is now possible because genotyping has become progressively cheaper and easier with large scanning datasets increasingly available.

Dr Konopka and colleagues used two sets of data to unravel the patterns of gene expression in the brain.

These included the results of bits of DNA called RNA in brain tissue from post mortems and the activity of neurons from epilepsy patients undergoing an EEG (electroencephalogram (EEG) in which a skull cap is worn.

Dr Konopka said: "We measure RNA as a proxy for gene expression in the brain. Quantitating RNA in the brain requires extracting RNA from the brain tissue itself.

"Thus, we are limited to accessing brain tissue post-mortem, or, in rare occasions, can obtain tissue from surgical resections of the brain."

The goal was to pinpoint genes important for 'normal cognition' such as learning and memory - both of which begin to fail as dementia develops.

Previous work has established certain groups of genes have altered gene expression in individuals with cognitive problems.
Dr Konopka said the genes they looked at in the subjects with epilepsy are not affected by the condition - meaning they will apply to the general population.

She said: "At this point, we cannot say whether the gene expression itself might drive memory or whether it's simply a reflection of the brain activity patterns needed for proper memory formation."
The memory genes also overlap with several linked to autism which offers new insights into that condition.

Dr Fedorenko said: "Given the inherently interdisciplinary nature of this emerging field of research, I hope many young neuroscientists and geneticists will get excited about possibilities of new critical discoveries and join our efforts by bringing in fresh energy and revolutionary ideas, so that together we can understand how genes give rise to our neural and cognitive architecture."

Alzheimer's is often diagnosed after people experience lapses in their memory, have difficulty remembering recent events and struggle to process new information.

Detecting the condition before it happens is the 'holy grail' for treatments and potential cures.

It is believed those born with certain genes have a predisposition to brain changes associated with dementia which affects 850,000 people in the UK alone - which will rise to one million by 2025.

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NCBS & inStem presents new insights into how brain responds to trauma

National Centre for Biological Sciences (NCBS) and the Institute for Stem Cell Biology and Regenerative Medicine (inStem) have gained insights into how a single instance of severe stress can lead to delayed and long-term psychological trauma.

The two Bengaluru-based research centres have indicated that a single stressful incident can lead to increased electrical activity in a brain region known as the amygdala. The activity is delayed, occurring 10 days after a single episode of stress, and is dependent on a molecule known as the N-Methyl-D-Aspartate Receptor (NMDA-R), a protein on nerve cells known to be crucial for memory functions.

The work pinpoints key molecular and physiological processes that could be driving changes in brain architecture. The amygdala is a small, almond-shaped groups of nerve cells located deep within the temporal lobe of the brain. This region of the brain is known to play key roles in emotional reactions, memory and making decisions. Changes in the amygdala are linked to the development of Post-Traumatic Stress Disorder (PTSD),.

The NCBS  team led by Prof. Sumantra Chattarji, was represented by Farhana Yasmin and Kapil Saxena along with  Bruce S. McEwen, head, Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology, The Rockefeller University, New York established that the new nerve connections in the amygdala lead to heightened electrical activity in this region of the brain.

Furthermore, a well-known protein involved in memory and learning, NMDA-R has been recognised as one of the agents that bring about these changes. Blocking the NMDA-R during the stressful period not only stopped the formation of new synapses, but  also blocked the increase in electrical activity at these synapses.

Previously, Chattarji’s group had shown that a single instance of acute stress had no immediate effects on the amygdala of rats. But 10 days later, these animals began to show increased anxiety, and delayed changes in the architecture of their brains, especially the amygdala.

“We showed that our study system is applicable to PTSD. This delayed effect after a single episode of stress was reminiscent of what happens in PTSD patients. We know that the amygdala is hyperactive in PTSD patients. But no one knows as of now, what is going on in there,” said Prof. Chattarji.

Investigations revealed major changes in the microscopic structure of the nerve cells in the amygdala. Stress seems to have caused the formation of new nerve connections called synapses in this region of the brain.

Prof. Chattarji’s group first began their investigations on  stress affecting  the amygdala and other regions of the brain around 10 years ago. The work required the team to employ an array of highly specialised and diverse procedures that range from observing behaviour to recording electrical signals from single brain cells and using an assortment of microscopy techniques.

“Now we have for the first time, a molecular mechanism that shows what is required for the culmination of events 10 days after a single stress,” said Prof. Chattarji.

“Most studies on stress are done on a chronic stress paradigm with repeated stress, or with a single stress episode where changes are looked at immediately afterwards, like a day after the stress,” said Yasmin.

“To do this, we need to use a variety of techniques and collaborations with experts We acknowledge the support of Wadhwani Foundation and DBT-DAE for funding this work,” he added.

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