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Brain-Blood Barrier might influence progression of Alzheimer's
Thursday, 01 October 2015

More and more data from preclinical and clinical studies strengthen the hypothesis that immune system-mediated actions contribute to and drive pathogenesis in Alzheimer's disease. The team of Roosmarijn Vandenbroucke in the Claude Libert Group (VIB/UGent) combined their knowledge and expertise related to inflammation with the expertise in Alzheimer's disease present in the Bart De Strooper Group (VIB/KU Leuven). This collaboration lead to the insights that Aβ indeed induces a strong inflammatory response, thereby destroying an important but often neglected brain barrier, called the blood-cerebrospinal fluid (CSF) barrier. Disruption of this blood-CSF barrier disturbs brain homeostasis and might negatively affect disease progression. Strikingly, these effects could be blocked in the presence of a matrix metalloproteinase (MMP) inhibitor.

Roosmarijn Vandenbroucke: "Although further research is needed, these data suggest that blocking MMP activity or upstream inflammatory signalling, might have therapeutic potential to treat Alzheimer's disease. It is important we could demonstrate the role of the blood-cerebrospinal fluid barrier, because this would be an easier target to reach in comparison with the targets of current therapies."

The publication of Vandenbroucke et al. was picked up by who combined it together with another publication about the Blood-Brain Barrier: Barriers Between Blood and CSF, Brain Yield to Aβ - Not a Bad Thing? 18 Sep 2015.

The barrier between the blood and central nervous system crumbles in Alzheimer's disease, but researchers have known little about how this happens, or what it does to brain pathology. Two new papers shed some light on how Aβ damages the cells that protect the brain parenchyma and cerebrospinal fluid. The studies examine different systems and describe distinct mechanisms, but both add to the picture of what may happen in disease.
Warm Hands, Warm Heart
Friday, 09 May 2014

People cooperate with each other more when they've been holding hot, as opposed to cold, objects.

This is the finding of a study by Simon Storey and Professor Lance Workman from the University of South Wales presented as part of the poster presentation session at the British Psychological Society's annual conference today, Thursday 8 May 2014, hosted at the International Convention Centre, Birmingham.

The Iterated Prisoner's Dilemma (IPD) task, designed to measure levels of cooperation, was completed by 60 students. Before performing the IPD task, participants were asked to hold either hot or cold objects.

Analysis showed that individuals who held hot objects cooperated significantly more frequently when they had held the hot, as opposed to cold, objects.

Professor Workman said: "There is evidence that, during our evolution, the part of the brain responsible for processing interpersonal warmth came to 'piggyback' on top of the part of the brain responsible for physical warmth. So when we say we have 'warmed to someone' this is, in a sense, literally true."

We used prisoner's dilemma because it is a well-established tool for measuring cooperation, but we suspect that simply by giving someone a sensation of warmth they are more likely to cooperate under other circumstances. Perhaps next time you need to ask someone for a favour it might be worth making them a cup of tea first!"

Full poster paper presentation title: 'Warm hand, warm heart: warm temperature priming increases cooperation on the Iterated Prisoner's Dilemma'.
PTSD: Could memory-rewriting drug help?
Sunday, 30 March 2014

A study conducted by neuroscientists at the Massachusetts Institute of Technology has looked at a new kind of drug that may be beneficial for people suffering from post-traumatic stress disorder.

Nearly 8 million Americans are currently suffering from post-traumatic stress disorder (PTSD), an anxiety disorder that some people who have been through distressing events suffer from.

Examples of the kind of traumatic events people with PTSD might have experienced include military combat, sexual assault, natural disasters (such as earthquakes or floods) or serious road accidents.

Not everyone who goes through a distressing event will get PTSD, but we know that it is common - nearly 20% of Vietnam veterans experienced PTSD after the war.

People who do have PTSD will usually be treated with psychotherapy. This is a talking therapy where the patient will talk through their experience with a trained therapist, with the goal of understanding and eventually overcoming their fear.

Psychotherapy does not always work, though, especially if the trauma the patient experienced occurred a long time ago. Doctors think this is because the traumatic experience becomes too "entrenched" in the patient's memory.

:Can traumatic memories be 'overwritten'?

The Massachusetts Institute of Technology (MIT) neuroscientists wanted to see if they could "extinguish" traumatic memories using a drug treatment. They tested a drug called a HDAC2 inhibitor - which is normally used to treat cancer - to see if the drug could remove fearful memories in mice.

To test this, the researchers first instilled a fear in the mice of a specific chamber in their habitat by administering a weak electric shock to their feet when they entered that chamber.

The researchers found that they could train the mice to overcome their fear of the chamber if they placed them within the chamber without administering the electric shock. But this only worked on mice whose memories of the electric shock were 24 hours old.

A second group of mice whose memories of the shock were 30 days old could not be trained to overcome their fear of the chamber.

Li-Huei Tsai, the director of MIT's Picower Institute for Learning and Memory, says:

"If you do something within this window of time, then you have the possibility of modifying the memory or forming a new trace of memory that actually instructs the animal that this is not such a dangerous place. However, the older the memory is, the harder it is to really change that memory."

Molecular memory

In the mice with the 24-hour-old memories, the researchers observed that, while the mice were being re-trained, the HDAC2 protein became inactive in their brains. This caused a process called histone acetylation to occur, which scientists think enables the brain to make new memories or "overwrite" old memories. But this process did not occur in the brains of the mice with the 30-day-old memories.

So the researchers decided to reduce the HDAC2 protein in the fearful mice using the HDAC2 inhibitors. When they did so, they found that the mice could be trained to overcome their 30-day-old fears of the chamber.

Publishing their findings in the journal Cell, the researchers think this explains the molecular reasons why older traumatic memories are harder to overcome than newer memories.

The researchers also noticed that the HDAC2 inhibitor drug seemed to "switch-on" genes that aid memory formation, and cause increased activity in the hippocampus of these mice - the area of the brain where memories are formed.

Prof. Tsai told Medical News Today that she hopes HDAC2 inhibitors will be investigated as a potential treatment for PTSD, phobias and anxiety disorders in humans:

"If there is no safety issue, I think HDAC2 inhibitors can be used in conjunction with psychotherapy as the first line treatment, as the combo enables much more efficient fear memory extinction, especially for the long-term, remote memories."

Written by David McNamee
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