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A study led by researchers at Cedars-Sinai and NeuroVision Imaging LLC provides a scientific basis for using noninvasive eye imaging to essentially detect signs of Alzheimer’s. The experimental technology, developed by Cedars-Sinai and NeuroVision, scans the retina using techniques that can identify beta-amyloid protein deposits that mirror those in the brain.
Accumulations of neurotoxic beta-amyloid protein can be detected with positron emission tomography, or PET scans, and analysis of cerebrospinal fluid. But these are invasive, inconvenient and costly, according to the study. making them impractical for routine screening and follow-up evaluation.
“This is the first study demonstrating the potential to image and quantify retinal findings related to beta-amyloid plaques noninvasively in living patients using a retinal scan with high resolution,” said Dr. Maya Koronyo-Hamaoui, an associate professor of neurosurgery and biomedical sciences and a research scientist at the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai, in a statement. Koronyo-Hamaoui is also a co-founder, inventor and scientist at NeuroVision. She is the senior leading author of an article in JCI Insight published online Aug. 17.
“This clinical trial is reinforced by an in-depth exploration of the accumulation of beta-amyloid in the retina of Alzheimer’s patients versus matched controls, and a comparison analysis between retina and brain pathologies,” she said. “Findings from this study strongly suggest that retinal imaging can serve as a surrogate biomarker to investigate and monitor Alzheimer’s disease,”
“As a developmental outgrowth of the central nervous system that shares many of the brain’s characteristics, the retina may offer a unique opportunity for us to easily and conveniently detect and monitor Alzheimer’s disease,” said Dr. Keith L. Black, chairman of NeuroVision, chair of the department of neurosurgery and director of the Maxine Dunitz Neurosurgical Institute at Cedars-Sinai, in a statement. “We know that Alzheimer’s begins as many as 10 or 20 years before cognitive decline becomes evident, and we believe that potential treatments may be more effective if they can be started early in the process. Therefore, screening and early detection may be crucial to our efforts to turn the tide against the growing threat of this devastating disease.”
Steven Verdooner, NeuroVision CEO, said in a statement that the imaging system harnesses the company’s expertise in autofluorescence imaging of the retina using a specialized ophthalmic camera and sophisticated image processing software.
“It’s exciting to see these studies demonstrating the power of the technology applied to the Alzheimer’s field,” said Verdooner. “Our goal is to develop a product that is easy to use, affordable and widely accessible. We look forward to the potential of retinal imaging playing a vital role in solving the problem of Alzheimer’s, both in identifying and monitoring those who may be affected by the disease. Our next step is to continue with clinical trials, building upon the existing pharmaceutical company collaborations, to ensure our technology is ready for the medical community to help manage this disease.”
The study’s first author, Yosef Koronyo, a research associate at Cedars-Sinai and a scientist and inventor at NeuroVision, said in a statement that the latest findings cap a decade of study that has produced several landmark discoveries.
“In 2010, our research group published an article providing the first evidence for the existence of Alzheimer’s-specific plaques in the human retina, and we demonstrated the ability to detect individual plaques in live mouse models using a modified ophthalmic device,” said Koronyo.
After adapting the technology for human application, the researchers kickstarted several ongoing clinical trials in the United States and Australia to determine the feasibility of detecting, and quantifying, beta-amyloid plaques in patients with the disease.
In the new article, the researchers report on a 16-patient clinical trial to demonstrate the feasibility of identifying beta-amyloid in the eye using autofluorescence imaging. They also provide detailed analyses and several new findings on Alzheimer’s pathology in the retina, results of research with donated eyes and brains of 37 deceased patients, 23 with confirmed Alzheimer’s disease and 14 controls.
The researchers reported a 4.7-fold increase in retinal plaque burden in patients with Alzheimer’s, compared to controls, and they provided observations regarding geometric distribution and layer location of amyloid pathology in the retina. With the imaging technology’s ability to detect autofluorescence signal related to retinal beta-amyloid, these findings may lead to a practical approach for large-scale identification of the at-risk population and monitoring of Alzheimer’s, the researchers said.
Funding for the study was provided by a National Institutes of Health/National Institute on Aging award, The Saban Family Foundation and The Marciano Family Foundation.
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A good night’s sleep does more than rejuvenate you for the next day. It may help protect you against Alzheimer’s disease. Research has begun to show an association between poor sleep and a higher risk of accumulating beta-amyloid protein plaque in the brain, one of the hallmarks of the disease.
Summary: Researchers have identified a neural circuit that is critical for memory retrieval.
Neuroscientists discover a brain circuit dedicated to retrieving memories.
When we have a new experience, the memory of that event is stored in a neural circuit that connects several parts of the hippocampus and other brain structures. Each cluster of neurons may store different aspects of the memory, such as the location where the event occurred or the emotions associated with it.
Neuroscientists who study memory have long believed that when we recall these memories, our brains turn on the same hippocampal circuit that was activated when the memory was originally formed. However, MIT neuroscientists have now shown, for the first time, that recalling a memory requires a “detour” circuit that branches off from the original memory circuit.
“This study addresses one of the most fundamental questions in brain research — namely how episodic memories are formed and retrieved — and provides evidence for an unexpected answer: differential circuits for retrieval and formation,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, the director of the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, and the study’s senior author.
This distinct recall circuit has never been seen before in a vertebrate animal, although a study published last year found a similar recall circuit in the worm Caenorhabditis elegans.
Dheeraj Roy, a recent MIT PhD recipient, and research scientist Takashi Kitamura are the lead authors of the paper, which appears in the Aug. 17 online edition of Cell. Other MIT authors are postdocs Teruhiro Okuyama and Sachie Ogawa, and graduate student Chen Sun. Yuichi Obata and Atsushi Yoshiki of the RIKEN Brain Science Institute are also authors of the paper.
The hippocampus is divided into several regions with different memory-related functions — most of which have been well-explored, but a small area called the subiculum has been little-studied. Tonegawa’s lab set out to investigate this region using mice that were genetically engineered so that their subiculum neurons could be turned on or off using light.
The researchers used this approach to control memory cells during a fear-conditioning event — that is, a mild electric shock delivered when the mouse is in a particular chamber.
Previous research has shown that encoding these memories involves cells in a part of the hippocampus called CA1, which then relays information to another brain structure called the entorhinal cortex. In each location, small subsets of neurons are activated, forming memory traces known as engrams.
“It’s been thought that the circuits which are involved in forming engrams are the same as the circuits involved in the re-activation of these cells that occurs during the recall process,” Tonegawa says.
However, scientists had previously identified anatomical connections that detour from CA1 through the subiculum, which then connects to the entorhinal cortex. The function of this circuit, and of the subiculum in general, was unknown.
In one group of mice, the MIT team inhibited neurons of the subiculum as the mice underwent fear conditioning, which had no effect on their ability to later recall the experience. However, in another group, they inhibited subiculum neurons after fear conditioning had occurred, when the mice were placed back in the original chamber. These mice did not show the usual fear response, demonstrating that their ability to recall the memory was impaired.
This provides evidence that the detour circuit involving the subiculum is necessary for memory recall but not for memory formation. Other experiments revealed that the direct circuit from CA1 to the entorhinal cortex is not necessary for memory recall, but is required for memory formation.
“Initially, we did not expect the outcome would come out this way,” Tonegawa says. “We just planned to explore what the function of the subiculum could be.”
“This paper is a tour de force of advanced neuroscience techniques, with an intriguing core result showing the existence and importance of different pathways for formation and retrieval of hippocampus-dependent memories,” says Karl Deisseroth, a professor of bioengineering and psychiatry and behavioral sciences at Stanford University, who was not involved in the study.
Why would the hippocampus need two distinct circuits for memory formation and recall? The researchers found evidence for two possible explanations. One is that interactions of the two circuits make it easier to edit or update memories. As the recall circuit is activated, simultaneous activation of the memory formation circuit allows new information to be added.
“We think that having these circuits in parallel helps the animal first recall the memory, and when needed, encode new information,” Roy says. “It’s very common when you remember a previous experience, if there’s something new to add, to incorporate the new information into the existing memory.”
Another possible function of the detour circuit is to help stimulate longer-term stress responses. The researchers found that the subiculum connects to a pair of structures in the hypothalamus known as the mammillary bodies, which stimulates the release of stress hormones called corticosteroids. That takes place at least an hour after the fearful memory is recalled.
While the researchers identified the two-circuit system in experiments involving memories with an emotional component (both positive and negative), the system is likely involved in any kind of episodic memory, the researchers say.
The findings also suggest an intriguing possibility related to Alzheimer’s disease, according to the researchers. Last year, Roy and others in Tonegawa’s lab found that mice with a version of early-stage Alzheimer’s disease have trouble recalling memories but are still able to form new memories. The new study suggests that this subiculum circuit may be affected in Alzheimer’s disease, although the researchers have not studied this.
ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE
Funding: The research was funded by the RIKEN Brain Science Institute, the Howard Hughes Medical Institute, and the JPB Foundation.
Source: Anne Trafton – MIT Image Source: NeuroscienceNews.com image is credited to Dheeraj Roy/Tonegawa Lab, MIT. Original Research:Abstract for “Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories” by Dheeraj S. Roy, Takashi Kitamura, Teruhiro Okuyama, Sachie K. Ogawa, Chen Sun, Yuichi Obata, Atsushi Yoshiki, and Susumu Tonegawa in Cell. Published online August 17 2017 doi:10.1016/j.cell.2017.07.013
Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories
•dSub and the circuit, CA1→dSub→EC5, are required for hippocampal memory retrieval
•The direct CA1→EC5 circuit is essential for hippocampal memory formation
•The dSub→MB circuit regulates memory-retrieval-induced stress hormone responses
•The dSub→EC5 circuit contributes to context-dependent memory updating
The formation and retrieval of a memory is thought to be accomplished by activation and reactivation, respectively, of the memory-holding cells (engram cells) by a common set of neural circuits, but this hypothesis has not been established.
The medial temporal-lobe system is essential for the formation and retrieval of episodic memory for which individual hippocampal subfields and entorhinal cortex layers contribute by carrying out specific functions.
One subfield whose function is poorly known is the subiculum. Here, we show that dorsal subiculum and the circuit, CA1 to dorsal subiculum to medial entorhinal cortex layer 5, play a crucial role selectively in the retrieval of episodic memories. Conversely, the direct CA1 to medial entorhinal cortex layer 5 circuit is essential specifically for memory formation.
Our data suggest that the subiculum-containing detour loop is dedicated to meet the requirements associated with recall such as rapid memory updating and retrieval-driven instinctive fear responses.
“Distinct Neural Circuits for the Formation and Retrieval of Episodic Memories” by Dheeraj S. Roy, Takashi Kitamura, Teruhiro Okuyama, Sachie K. Ogawa, Chen Sun, Yuichi Obata, Atsushi Yoshiki, and Susumu Tonegawa in Cell. Published online August 17 2017 doi:10.1016/j.cell.2017.07.013
Over the years, I have experienced family and friends dying of cancer. I observed their lifestyle and toxins they are exposed to. So to answer my friend’s question on how to detox and the mechanism of cleaning our body or getting rid of toxins, I listed some items for Dos and Donts.
Our lymphatic system which travels opposite our blood is responsible for cleaning our blood. Search for lymphatic, massage and detox in this site http://www.clubalthea.com
When we clean the many bad foods or toxins that entered our body, we must clean our liver first, our laboratory. It is closely linked to our heart that during our last breath, our liver is the first and last signal that our heart gets to shut down.
Detox or cleaning our cells from toxins is the key to living longer, the anti-aging process we all are seeking for. In my 50s, I could have died long time ago if I was born centuries ago with no clean water, fresh produce and raising a dozen children. Each child is minus 5 years of a woman’s age.
Detox is like cleaning the toilet. The following are detox tips and anti-aging tips to clean your cells:
Dos in cleansing your body from toxin, also detoxes your liver
Baking soda (pinch in your drinking water)
Digestive enzymes from pineapple and papaya
Apple cider vinegar
Wash produce with salt or diluted vinegar
No over ripe fruits and left over foods or 3-day old rice ( aflatoxin , mycotoxin )
No charred BBQ
Whole foods ; sulfur rich as they are anti-inflammatory (ginger, garlic, turmeric, coconut, walnuts)
Deep breathing thru nose and blow out thru mouth
Prayer: May God’s light energy be with you and say Amen to accept it.
Resveratrol from Berries, kiwi, citrus fruit
Donts are ways that when practiced or consumed can kills our nerve cells and produce toxins in our cells.
Avoidance of too much caffeine, iron and sugar, these are food for cancer
Other metal toxins
Plastics in food
Shift work: not sleeping from 10pm to 4 am
Over medications, chemo, other carcinogens
Avoid exposure to fumes, chemicals (formaldehydes,carcinogens,toxins)
And what is your recipe for liver detox and the mechanism by which it works to accomplish that?
From: Male friend in his late 50s whose brother died of pancreatic cancer