Alzheimer’s Disease: Possibly Caused From Haywire Immune System Eating Brain Connections?

By: Alexandria Addesso

Memory loss and absent-mindedness has long been seen as an inevitable flaw that comes with old age. Although there is a slew of medications on the market that are prescribed for those suffering from Alzheimer’s Disease, none seem to change it by too large of a margin. This has led scientists to rethink what in particular is the root cause of Alzheimer’s.

New studies done on laboratory test rodents have found that there is a marked loss of synapses, which are a junction between two nerve cells, consisting of a minute gap across which impulses pass by diffusion of a neurotransmitter. Specifically synapses that are located in brain regions that are highly significant and key to memory.



These junctions between nerve cells are where neurotransmitters are released to spark the brain’s electrical activity. Currently, all pharmaceutical drugs on the market for the treatment of Alzheimer’s, focus on eliminating β amyloid, a protein that forms telltale sticky plaques around neurons in people with the disease. But, more β amyloid does not always mean more severe symptoms such as memory loss or poor attention.

Researchers at the University of Virginia, School of Medicine, in Charlottesville found that a protein called ‘C1q’ sets off a series of chemical reactions that ultimately mark a synapse for destruction. After this occurs immune cells called microglia-glial cells derived from mesoderm that function as macrophages (scavengers) in the central nervous system and form part of the reticuloendothelial system, destroy or “eat” the synapse.



“It is beautiful new work brings into light what’s happening in the early stage of the disease,” said one of the researchers at the University of Virginia School of Medicine neuroscientist Jonathan Kipnis.

These findings could mean that treatment that blocks C1q could be pivotal and highly successful in fighting Alzheimer’s Disease. When researchers gave the laboratory rodent test subjects an antibody to stop the destruction of cells by microglia, synapse loss did not appear. This could also mean a slowing in cognitive decline, but according to Edward Ruthazer, a neuroscientist at the Montreal Neurological Institute and Hospital in Canada, using microglia as such a central role to fight the disease is “still on the controversial side.”

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The Possible Cause of Flashbacks Discovered

Traumatic events can stop the brain storing the context in which they took place.

Remembering the past is an important function and defines who we are. In some situations though, the normal processes that store our experiences into memory can go wrong. After experiencing a distressing event, people can develop memory disturbances where they re-experience the event in the form of flashbacks – distressing vivid images that involuntarily enter consciousness, as happens in post-traumatic stress disorder.

Our latest study shows that a distressing experience has opposite effects in two different parts of the brain: the amygdala and the hippocampus. The amygdala, a region of the brain involved in emotion, seemed to strongly encode the negative content of an experience while the hippocampus, which is involved in storing new memories, is only weakly activated.

When remembering something from the past, we can bring to mind what we were doing, the people we were with, and where the event took place. An important aspect of memory is that these separate pieces of information are bound together as a single memory so that all of it can easily be recalled at a later time. But when experiencing a distressing event, the normal processes that help to integrate this information in memory can be disrupted.

The hippocampus is crucial for forming these associations so that all parts of a memory can be later retrieved as a single event (and damage to this brain region can stop a person from forming new memories). In contrast, the amygdala is involved in processing emotional information and making basic responses to things associated with fear, such as recoiling from a snake or spider.


The hippocampus. The brain region involved in consolidating new memories.

People who have suffered a trauma often have difficulty remembering the context of the event. We thought that, while processing in the amygdala might be increased during a negative experience, processing in the hippocampus might be decreased, disrupting the way it binds the different aspects of the experience together as a single memory.

To test this idea we showed 20 volunteers pairs of pictures and asked them to remember the pictures while lying in an MRI scanner. Some of the pictures were of traumatic
scenes, such as a badly injured person.

The volunteers’ memory of the pictures was then tested in two ways. First, they were shown one picture from each pair and asked if they recognized previously seeing it. Second, if the picture was recognized, we then asked whether they could remember what other picture had been part of the original pair.

When asked whether they recognized the individual pictures, people showed better memory for previously seen pictures that were negative (traumatic) compared with pictures that were neutral, such as a person sitting at an office desk. Improved memory for negative pictures related to increased activity in the amygdala. In contrast, their memory for remembering what pictures were presented together as a pair was worse when one of the pictures was negative.



We also found that activity in the hippocampus was reduced by the presence of negative pictures suggesting that its function in storing the associations between the pictures was impaired. This imbalance could lead to strong memories for the negative content of an event that is not properly stored with the other parts of the event and the context in which it took place.

Implications for psychotherapy
This work supports the view that experiencing a traumatic event might alter how memory works. The re-experiencing of intrusive images in post-traumatic stress disorder might happen because of strengthened memory for the negative aspects of a trauma but not their context – that is, the location where the event occurred or the time it occurred. This may result in the person involuntarily retrieving the traumatic event “out of context” and experiencing it as though it was in the present.

In this case, therapy should focus on strengthening or recreating appropriate contextual associations for the negative event. This view is supported by current psychotherapies where a person is taken back to the place where the traumatic event took place to help in strengthening memory for the context.

These findings also highlight potential issues with eyewitness testimony as trauma sufferers with poorly contextualized memories are likely to provide a fragmented report of an event.

The author of this James Bisby, Research Associate, University College London. This article was originally published in The Conversation under a Creative Commons Attribution

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Our Cognitive process is in danger?

The Internet is increasingly taking over human memory

Our increasing reliance on the Internet and the ease of access to the vast resource available online is affecting our thought processes for problem solving, recall and learning. In a new article published in the Journal Memory, researchers at the University of California, Santa Cruz and University of Illinois, Urbana Champaign have found that 'cognitive offloading', or the tendency to rely on things like the Internet as an aide-mémoire, increases after each use.

We might think that memory is something that happens in the head but increasingly it is becoming something that happens with the help of agents outside the head. Benjamin Storm, Sean Stone & Aaron Benjamin conducted experiments to determine our likelihood to reach for a computer or smartphone to answer questions. Participants were first divided into two groups to answer some challenging trivia questions -- one group used just their memory, the other used Google. Participants were then given the option of answering subsequent easier questions by the method of their choice.



The results revealed that participants who previously used the Internet to gain information were significantly more likely to revert to Google for subsequent questions than those who relied on memory. Participants also spent less time consulting their own memory before reaching for the Internet; they were not only more likely to do it again, they were likely to do it much more quickly. Remarkably 30% of participants who previously consulted the Internet failed to even attempt to answer a single simple question from memory.

Lead author Doctor Benjamin Storm commented, "Memory is changing. Our research shows that as we use the Internet to support and extend our memory we become more reliant on it. Whereas before we might have tried to recall something on our own, now we don't bother. As more information becomes available via smartphones and other devices, we become progressively more reliant on it in our daily lives."



This research suggests that using a certain method for fact finding has a marked influence on the probability of future repeat behaviour. Time will tell if this pattern will have any further reaching impacts on human memory than has our reliance on other information sources.

Certainly the Internet is more comprehensive, dependable and on the whole faster than the imperfections of human memory, borne out by the more accurate answers from participants in the internet condition during this research. With a world of information a Google search away on a smartphone, the need to remember trivial facts, figures, and numbers is inevitably becoming less necessary to function in everyday life.

Source: Taylor & Francis

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A new way to Improve Memory is Discovered

Electrically Stimulating the Brain during Sleep
According to researchers, transcranial alternating current stimulation may help to improve memory when targeted to a specific kind of brain activity achieved during sleep.

By targeting one face of the brain’s electrical activity, UNC neuroscientist Flavio Frohlich showed it’s possible to enhance memory, laying the groundwork for a new treatment paradigm for neurological and psychiatric disorders.

When you sleep, your brain is busy storing and consolidating things you learned that day, stuff you’ll need in your memory toolkit tomorrow, next week, or next year. For many people, especially those with neurological conditions, memory impairment can be a debilitating symptom that affects every-day life in profound ways. For the first time, UNC School of Medicine scientists report using transcranial alternating current stimulation, or TACS, to target a specific kind of brain activity during sleep and strengthen memory in healthy people.



The findings, published in the journal Current Biology, offer a non-invasive method to potentially help millions of people with conditions such as autism, Alzheimer’s disease, schizophrenia, and major depressive disorder.

For years, researchers have recorded electrical brain activity that oscillates or alternates during sleep; they present as waves on an electroencephalogram (EEG). These waves are called sleep spindles, and scientists have suspected their involvement in cataloging and storing memories as we sleep.



“But we didn’t know if sleep spindles enable or even cause memories to be stored and consolidated,” said senior author Flavio Frohlich, PhD, assistant professor of psychiatry and member of the UNC Neuroscience Center. “They could’ve been merely byproducts of other brain processes that enabled what we learn to be stored as a memory. But our study shows that, indeed, the spindles are crucial for the process of creating memories we need for every-day life. And we can target them to enhance memory.”

This marks the first time a research group has reported selectively targeting sleep spindles without also increasing other natural electrical brain activity during sleep. This has never been accomplished with TDCS – transcranial direct current stimulation – the much more popular cousin of TACS in which a constant stream of weak electrical current is applied to the scalp.

During Frohlich’s study, 16 male participants underwent a screening night of sleep before completing two nights of sleep for the study.

Before going to sleep each night, all participants performed two common memory exercises – associative word-pairing tests and motor sequence tapping tasks, which involved repeatedly finger-tapping a specific sequence. During both study nights, each participant had electrodes placed at specific spots on their scalps. During sleep one of the nights, each person received TACS – an alternating current of weak electricity synchronized with the brain’s natural sleep spindles. During sleep the other night, each person received sham stimulation as placebo.



Each morning, researchers had participants perform the same standard memory tests. Frohlich’s team found no improvement in test scores for associative word-pairing but a significant improvement in the motor tasks when comparing the results between the stimulation and placebo night.

“This demonstrated a direct causal link between the electric activity pattern of sleep spindles and the process of motor memory consolidation.” Frohlich said.

Caroline Lustenberger, PhD, first author and postdoctoral fellow in the Frohlich lab, said, “We’re excited about this because we know sleep spindles, along with memory formation, are impaired in a number of disorders, such as schizophrenia and Alzheimer’s. We hope that targeting these sleep spindles could be a new type of treatment for memory impairment and cognitive deficits.”



Frohlich said, “The next step is to try the same intervention, the same type of non-invasive brain stimulation, in patients that have known deficits in these spindle activity patterns.”

Frohlich’s team previously used TACS to target the brain’s natural alpha oscillations to boost creativity. This was a proof of concept. It showed it was possible to target these particular brain waves, which are prominent as we create ideas, daydream, or meditate. These waves are impaired in people with neurological and psychiatric illnesses, including depression.

Source: University of North Carolina School of Medicine.

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Brain Function and Memory could be Modified

Researchers have developed a new tool that can modify brain activity and memory in targeted ways without the help on any chemicals or drugs.

Scientists at USC (University of Southern California) have developed a new tool to modify brain activity and memory in targeted ways, without the help of any drugs or chemicals.

The GFE3 protein may help researchers map the brain’s connections and better understand how inhibitory synapses modulate brain function, said lead author Don Arnold, a professor of biological sciences at the USC Dornsife College of Letters, Arts and Sciences.



It also may enable them to control neural activity and lead to advancements in research for diseases or conditions ranging from schizophrenia to cocaine addiction, Arnold said.

The new tool is a protein that carries a death sentence for synaptic proteins in specific cells. The protein can be encoded in animal genomes to effectively switch off their inhibitory synapses — connections between neurons — thus, increasing their electrical activity.

“GFE3 harnesses a little known and remarkable property of proteins within the brain,” Arnold said.

Hijacking the process

The protein takes advantage of an intrinsic process — the brain’s cycle of degrading and replacing proteins. Most brain proteins last only a couple of days before they are actively degraded and replaced by new proteins. GFE3 targets proteins that hold inhibitory synapses together to this degradation system and as a result, the synapses fall apart.

“Rather than a cell deciding when a protein needs to be degraded, we sort of hijack the process,” Arnold said.

A neuron with synapses, left, undergoes a change after the new protein is encoded, center, resulting in the synapses being degraded. The effect of the protein is then reversed.



For the study published in the journal Nature Methods, the team of scientists studied the protein’s effect in both mice and zebrafish. The researchers found that GFE3 protein triggered the neurons on the two sides of the spine to work in opposition, generating uncoordinated movements.

Previously, drugs could be used to inhibit inhibitory synapses in the brain, such as benzodiazapines, which treat anxiety, insomnia or seizures. But the drugs inhibit all the cells in a particular area, not just the neurons that are the intended target.

“Unfortunately, cells that have very different, even opposite functions tend to be right next to each other in the brain,” Arnold said. “Thus, pharmacological experiments are especially difficult to interpret. By encoding GFE3 within the genome, we can target and modulate the inhibitory synapses of specific cells without affecting other cells that have different functions.”



Source: Emily Gersema, Neuroscience News

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