Cells' garbage disposal may hold key to healthier life

October 3, 2016

Autophagy, the little-understood method by which human cells dispose of harmful waste and unwelcome intruders, may one day be central to therapies for longer, healthier living, experts said.

Japanese cell biologist Yoshinori Ohsumi was awarded the 2016 Nobel Medicine Prize Monday for discovering genes involved in autophagy, a non-stop housecleaning process that keeps cells healthy, and is thought to spur ageing and disease when disrupted.

Scientists are striving to "find a way to increase it beyond what it normally does," said University of Edinburgh cell biologist Simon Wilkinson referring to future treatment possibilities for cancer and neurodegenerative diseases such as Alzheimer's or Parkinson's.

"Can we find drugs that will ramp it up further than it would ordinarily be?" he told AFP by phone. "Can we ameliorate these horrible disorders?"

Trial drugs in lab experiments with human cells and mice have shown that autophagy can indeed be boosted.

In "mouse models, for example, where autophagy has been increased genetically, the mice do age better," Wilkinson said. 

Concretely, this meant a less rapid accumulation of damaged proteins in cells, and a metabolism with a slower rate of age-related decline.

Autophagy—from the Greek words for "self" and "to eat"—is a process by which cells in animals and plants get rid of damaged proteins, as well as specialised structures called organelles which have become defunct.

Allowed to accumulate, these useless scraps would damage the cell and upset its normal functioning, leading to health problems. 

Autophagy was already known to scientists in the 1960s, but Ohsumi, who studied the process in yeast in the 1990s, was the first to uncover the genes responsible.

Yeast is a favourite of biologists because it shares much of its cell structure and functioning with humans and other animals.

No drug in sight

Autophagy happens when fatty membranes called autophagosomes envelop the unwanted waste and sequester it from the rest of the cell. 

The autophagosomes then join up with another specialised cell compartment full of digestive enzymes, called a vacuole, to obliterate the waste.

"Autophagy declines when we age. That's why we accumulate these dysfunctional proteins that cause diseases," University of Warwick autophagy expert Ioannis Nezis told AFP.

"Now we are trying to understand how this process declines during ageing, and how we can find innovations to activate this process and keep our cells healthy for longer, so we can live a better and longer life."

The experts stressed that an autophagy-based drug was still far off.

"Tests are being conducted on mice," said Guido Kroemer, an autophagy researcher at the Inserm medical research institute. "Tests on humans might begin in a few years."

Two main avenues were being investigated, he explained. 

The first was an autophagy stimulator to slow ageing and the development of diseases such as diabetes, clogged arteries, certain cancers or neurodegenerative conditions. 

Another option was to use autophagy inhibitors to lower cancer cells' resistance to chemotherapy.

Much more is understood about autophagy since Ohsumi's breakthrough—with about a dozen papers published on the subject until 1990, and some 30,000 since then, according to Nezis.

But a lot remains unknown—chiefly how and when to use a drug molecule to boost autophagy without causing unwanted side-effects.

Wilkinson cautioned autophagy was unlikely to yield the elixir of life.

"This is an increase in health during ageing, it's not immortality by any stretch," he said.

"Inevitably, there will come a point where the autophagy process is finite... where the fundamental capacity of cells is just overcome by ageing-related damage."

http://medicalxpress.com/news/2016-10-cells-garbage-disposal-key-healthier.html

Dopamine Connected to Facial Recognition

NEUROSCIENCE NEWSOCTOBER 3, 2016

Summary: A new neuroimaging study has uncovered a link between dopamine and facial recognition.

Source: UT Dallas.

In a recent study, researchers at UT Dallas’ Center for BrainHealth, working in collaboration with colleagues in Sweden, have revealed a link between the dopamine neurotransmitter system in the brain and an individual’s ability to recognize faces. 

Led by Dr. Bart Rypma, Meadows Foundation Chair in the School of Behavioral and Brain Sciences, the study found that the amount of dopamine relative to the amount of brain activity in the fusiform gyrus strongly predicted the ability to recognize faces. Although the fusiform gyrus has been previously established as an area of the brain related to facial recognition, this is the first time scientists have made a connection between dopamine and facial recognition.

The findings were published in The Journal of Neuroscience. Dr. Nicholas Hubbard, who worked with Rypma, at the Center for BrainHealth, was a co-author of the paper.

“There is an intimate relationship between face recognition and the reward system,” said Rypma, associate professor of cognitive neuroscience and cognitive psychology. “For example, you can imagine that the more sensitive someone is to social rewards, the better they feel during social interactions with familiar faces. People who are better at recognizing faces are likely more socially outgoing than those who have greater trouble differentiating one face from another.”

Using a combination of functional magnetic resonance imaging (fMRI) and positron emission tomography (PET) imaging, researchers discovered that individuals who showed more brain activity per unit of dopamine showed better facial recognition.

Dopamine is the “feel-good” chemical linked to the body’s natural reward system. That system drives survival, providing individuals with motivation and rewards in the form of positive stimuli for vital behaviors such as eating nutritious food and procreating.

Dopamine is the “feel-good” chemical linked to the body’s natural reward system. That system drives survival, providing individuals with motivation and rewards in the form of positive stimuli for vital behaviors such as eating nutritious food and procreating. Neurosciencenews image is for illustrative 

purposes only

For the study, 10 male and 10 female participants, ages 22 to 30, were shown 24 faces and asked to remember them.

Participants then underwent fMRI scanning while they were shown the studied faces intermixed with new ones. As participants viewed each face, they were asked to indicate whether it was new or familiar while the researchers monitored their brain activity. Researchers also measured dopamine availability of each participant with a PET scan. 

“The findings suggest that the strength of the neural response to the amount of dopamine transmitted could be key to understanding why we remember some faces and forget others,” Hubbard said. “Establishing this empirical link between fusiform activity and dopamine binding, and linking these to a cognitive process that is highly relevant for survival in a social world, was a most exciting find.”

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Significant portions of the study were completed while Rypma was in residence at the Aging Research Center of the Karolinska Institutet in Stockholm. 

Funding: The work was supported by The University of Texas at Dallas Faculty Development Leave program; the National Institutes of Health; the Swedish Research Council; Swedish Council for Working Life and Social Research; Swedish Brain Power, an Alexander von Humboldt Research Award; and a donation from the af Jochnick Foundation, and the Torsten and Ragnar Söderberg’s Foundation.

Source: Emily Bywaters – UT Dallas

Image Source: This NeuroscienceNews.com image is in the public domain.

Original Research: Full open access research for “Dopamine D1 Binding Potential Predicts Fusiform BOLD Activity during Face-Recognition Performance” by Bart Rypma, Håkan Fischer, Anna Rieckmann, Nicholas A. Hubbard, Lars Nyberg, and Lars Bäckman in Journal of Neuroscience. Published online October 2016 doi:10.1523/JNEUROSCI.1298-15.2015

CITE THIS NEUROSCIENCENEWS.COM ARTICLE

Abstract

The neural networks of subjectively evaluated emotional conflicts

The importance of face memory in humans and primates is well established, but little is known about the neurotransmitter systems involved in face recognition. We tested the hypothesis that face recognition is linked to dopamine (DA) activity in fusiform gyrus (FFG). DA availability was assessed by measuring D1 binding potential (BP) during rest using PET. We further assessed blood-oxygen-level-dependent (BOLD) signal change while subjects performed a face-recognition task during fMRI scanning. There was a strong association between D1 BP and BOLD activity in FFG, whereas D1 BP in striatal and other extrastriatal regions were unrelated to neural activity in FFG. These results suggest that D1 BP locally modulates FFG function during face recognition. Observed relationships among D1 BP, BOLD activity, and face-recognition performance further suggest that D1 receptors place constraints on the responsiveness of FFG neurons.

SIGNIFICANCE STATEMENT The importance of face memory in humans and primates is well established, but little is known about the neurotransmitter systems involved in face recognition. Our work shows a role for a specific neurotransmitter system in face memory.

“Dopamine D1 Binding Potential Predicts Fusiform BOLD Activity during Face-Recognition Performance” by Bart Rypma, Håkan Fischer, Anna Rieckmann, Nicholas A. Hubbard, Lars Nyberg, and Lars Bäckman in Journal of Neuroscience. Published online October 2016 doi:10.1523/JNEUROSCI.1298-15.2015

http://neurosciencenews.com/facial-recognition-dopamine-5177/

Google’s Verily lends tech to Parkinson’s study

3 October 2016

Verily’s Jessica Mega

Google’s life sciences division Verily is to play a part in an observational Parkinson’s disease study.

The company is to work with Radboud University Medical Center, Radboud University in Nijmegen, Netherlands, and ParkinsonNet to examine the progression of Parkinson’s disease in a study group of 650 patients.

The study aims to gain insights into the origin and progression of the disease in each individual in order to build more personalised treatments.

The study will use advanced brain imaging and molecular analysis techniques to provide real-time data from each patient alongside wearable devices to collect activity and vital signs data.

Currently, around 44,000 people in the Netherlands are living with Parkinson’s disease. Worldwide, more than 10 million are affected – a number expected to increase with an ageing worldwide population.

“The disease symptoms, disease progression, and treatment response in Parkinson’s disease vary considerably among patients,” said Bastiaan Bloem, professor of neurological movement disorders and founder of ParkinsonNet. “Currently, we don’t understand what causes these differences and therefore we cannot offer patients a treatment plan that is tailored to their individual needs.”

Verily’s exact involvement in the study is not specified, although there have been reports of the company developing a health-focused smartwatch that will focus on measuring both heart rate and activity levels. Whether the watch will feature in the study has not been confirmed.

“We are excited to bring Verily’s unique tools and technology to this collaboration in order to more deeply understand Parkinson’s disease and discover new insights,” commented Jessica Mega, chief medical officer at Verily. “This partnership is illustrative of our commitment to Parkinson’s disease and other neurological disorders, such as multiple sclerosis. We are working with leading researchers on studies like this one to better understand disease progression and to improve the lives of patients.”

This latest collaboration continues Verily continues progress in forging partnerships in the healthcare sector. Last month, the company teamed with Sanofi to establish a joint diabetes management venture by the name of Onduo. Prior to that, the company joined forces with GlaxoSmithKline to create a bioelectronics medicines-dedicated company called Galvani Bioelectronics.

Data collected from the study will be made freely available to participating Dutch hospitals to allow them to carry out their own research into the disease. Researchers from outside the Netherlands will also have the opportunity to use the data upon the submission of a research proposal.

http://pharmaphorum.com/news/googles-verily-lends-tech-dutch-parkinsons-study/?

GLNT and UCB Partner to Create Ways to Better Judge Effectiveness of Parkinson’s Treatment

OCTOBER 3, 2016, BY CAROLINA HENRIQUES IN NEWS.

Great Lakes NeuroTech (GLNT) announced that it will partner with UCB to develop quantitative tools that will help Parkison’s disease (PD) patients and their clinicians to better assess the impact of  treatment. The goal is to improve patients’ individual experiences as well as, ultimately, improve their quality of life.

Parkinson’s disease causes tremors, and impaired mobility and movement, as well as additional side effects to medication that can include involuntarily movements. These symptoms are challenging to patients, regardless of their intensity. Being able to access detailed feedback on how a patient responds to treatment could give clinicians the tools needed to improve patients care and to tailor treatments to suit individual needs.

Under the partnership, the companies will combine data from wearable diagnostics (like sensors and apps) and therapy dosage, and turn them into visualization feedback tools. This may help clinicians to adjust dosages to optimal settings, and guide patient feedback to confirm that the therapy is achieving best possible results.

“Simply putting ambulatory sensors on a patient is no longer that difficult. What is incredibly challenging, rewarding and distinguishes GLNT is developing targeted algorithms and applications which can use that data to actually guide clinical decisions,” Joe Giuffrida, GLNT’s president, said in a press release. “Our research team has spent years developing and validating algorithms for assessing motor symptoms, and are excited to now partner with UCB on a targeted therapy application.”

In a planned pilot study to explore the companies’ combined expertise:

• UCB will bring its Neupro (transdermal system) therapy, a Parkinson’s-specific skin patch that releases rotigotine, a dopamine agonist, continuously for 24 hours.
• GLNT will bring its Kinesia system for objective, wearable assessment of Parkinson’s motor symptoms. Kinesia uses sensors and apps to monitor symptoms remotely. The system has been validated in more than 100 publications, and has been cleared for use by the U.S. Food and Drug Administration (FDA) as well as by the European Medicines Agency (EMA).

“UCB is committed to identifying and addressing the unmet needs of people living with Parkinson’s Disease to enable them to have a more engaged life every day,” said Ana Infante, head of UCB’s Free Motion Mission. “We are excited to be collaborating with GLNT to progress and explore value creating opportunities in movement disorders and other neurological diseases of high unmet need. This partnership supports our vision of ensuring all patients with movement disorders experience an optimum treatment experience.”

http://parkinsonsnewstoday.com/2016/10/03/great-lakes-neurotech-ucb-partner-to-create-ways-of-judging-parkinsons-treatment-effect

Coronavirus and neurological disease: Direct link

October 3, 2016 (Updated Oct. 4, 2016)

Source:

Institut national de la recherche scientifique - INRS

Summary:

For the first time, researchers have found proof of a direct association between strain OC 43 of the human coronavirus (HCoV) and neurological disease in humans. Researchers suggest the neuropathological effects of this virus are responsible for approximately 20% of common colds and more severe respiratory conditions in certain vulnerable individuals

Credit: Institut national de la recherche scientifique

For the first time, researchers have found proof of a direct association between strain OC 43 of the human coronavirus (HCoV) and neurological disease in humans. This breakthrough was made by British and Quebec researchers, including Professor Pierre Talbot of the INRS-Institut Armand-Frappier Centre, who was the first not only to demonstrate the virus's ability to invade the human central nervous system, but also to suggest the neuropathological effects of this virus responsible for approximately 20% of common colds and more severe respiratory conditions in certain vulnerable individuals. The discovery was recently featured in the New England Journal of Medicine.

The researchers studied the case of a very young patient who died from encephalitis. The patient had presented severe immunodeficiency and received a stem cell transplant. Although most cases of encephalitis are caused by viruses or bacteria, it can be particularly difficult to pinpoint the cause in immunodeficient patients. As the case study shows, it was impossible to identify the pathogen using conventional techniques.

The researchers used various methods that allowed them to irrefutably identify the presence of strain OC-43 of the human coronavirus in the young patient's brain tissue. "Among the methods used, deep sequencing of biopsy materials provides an important tool for the diagnosis of unexplained encephalitis, particularly in immunodeficient patients who have undergone stem cell transplantation," said Professor Talbot. This breakthrough is significant because it will make it possible to use specific treatments that are better tailored to patient conditions.

The results obtained confirm Professor Talbot's hypothesis that the human respiratory coronavirus can cause certain neurological diseases of unknown origin, such as multiple sclerosis, Alzheimer's disease, Parkinson's disease, and encephalitis.

Story Source:

Materials provided by Institut national de la recherche scientifique - INRS. Original written by Gisèle Bolduc. Note: Content may be edited for style and length.

---

Journal Reference:

1. Sofia Morfopoulou, Julianne R. Brown, E. Graham Davies, Glenn Anderson, Alex Virasami, Waseem Qasim, Wui K. Chong, Michael Hubank, Vincent Plagnol, Marc Desforges, Thomas S. Jacques, Pierre J. Talbot, Judith Breuer. Human Coronavirus OC43 Associated with Fatal Encephalitis. New England Journal of Medicine, 2016; 375 (5): 497 DOI: 10.1056/NEJMc1509458

https://www.sciencedaily.com/releases/2016/10/161003114804.htm

Out of the limelight: Nobel medicine prize winner Ohsumi

October 3, 2016

Some people are drawn to the flashy and popular, but Nobel laureate Yoshinori Ohsumi isn't one of them.

The 71-year-old Japanese scientist won the 2016 prize in medicine on Mondayfor his "brilliant" work on how damaged cells recycle themselves—known as autophagy—and the major implications it has for health and diseases, including cancer and neurological disorders.

But Ohsumi's field of interest was far from the limelight when he started his career.

Winning the Nobel "was my childhood dream, but it has not been the focus of my concern since I got into research—I don't like competing", Ohsumi told a press briefing in Tokyo Monday evening.

"I have fun doing what others don't do, rather than something that everybody is flocking to."

In response to questions, he said he was worried about budget cutbacks in scientific research.

"It's fun to do (research) without knowing where things will go," he added.

Born in southwest Fukuoka near the end of World War II, Ohsumi was initially interested in chemistry, but switched his focus to molecular biology, according to a 2012 interview.

Ohsumi—the youngest of four brothers—received a PhD from the University of Tokyo in 1974 and spent several years at Rockefeller University in New York before coming back to Japan in the late 1980s.

He has been a professor at the Tokyo Institute of Technology since 2009.

In what the jury described as a "series of brilliant experiments in the early 1990s", Ohsumi used baker's yeast to identify genes essential for autophagy.

He then went on to explain the underlying mechanisms for autophagy in yeast and showed that similar sophisticated machinery is used in human cells.

Ohsumi's findings opened the path to understanding the importance of autophagy in many physiological processes, such as how the body adapts to starvation or responds to infection.

When autophagy breaks down, links have been established to Parkinson's disease, type 2 diabetes and other disorders that appear in the elderly.

"Autophagy has been known for over 50 years but its fundamental importance in physiology and medicine was only recognised after Yoshinori Ohsumi's paradigm-shifting research in the 1990's," the Nobel jury said Monday.

Ohsumi is the 25th Japanese person to win a Nobel Prize, and the fourth in the medicine category, according to local media.

Last year, Japan's Satoshi Omura shared the Nobel Prize medicine with two scientists from Ireland and China for unlocking treatments for malaria and roundworm.

In 2012, Shinya Yamanaka shared the medicine prize with Britain's John B. Gurdon for discoveries showing how adult cells can be transformed back into stem cells.

http://medicalxpress.com/news/2016-10-limelight-nobel-medicine-prize-winner.html

Japan's Ohsumi wins Nobel for studies of cell 'self-eating'

October 3, 2016

Nobel Prize winner Yoshinori Ohsumi smiles as he speaks with Japanese Prime Minister Shinzo Abe on a mobile phone during a press conference at the Tokyo Institute of Technology in Tokyo Monday, Oct. 3, 2016. Ohsumi won the Nobel Prize in medicine on Monday for discoveries on how cells break down and recycle content, a garbage disposal system that scientists hope to harness in the fight against cancer, Alzheimer's and other diseases. (AP Photo/Shizuo Kambayashi)

Japanese biologist Yoshinori Ohsumi won the Nobel Prize in medicine on Monday for discoveries on how cells break down and recycle content, a garbage disposal system that scientists hope to harness in the fight against cancer, Alzheimer's and other diseases.

The Karolinska Institute honored Ohsumi for "brilliant experiments" in the 1990s on autophagy, a phenomenon that literally means "self-eating" and describes how cells gobble up damaged content and provide building blocks for renewal.

Disrupted autophagy (aw-TAH'-fuh-jee) has been linked to several diseases including Parkinson's, diabetes and cancer, the prize committee said.

"Intense research is now ongoing to develop drugs that can target autophagy in various diseases," it said in its citation .

Ohsumi, 71, from Fukuoka, Japan, is a professor at the Tokyo Institute of Technology. In 2012, he won the Kyoto Prize, Japan's highest private award for global achievement.

Ohsumi said he never thought he would win a Nobel Prize for his work, which he said involved studying yeast in a microscope day after day for decades.

"As a boy, the Nobel Prize was a dream, but after starting my research, it was out of my picture," he told reporters in Tokyo.

"I don't feel comfortable competing with many people, and instead I find it more enjoyable doing something nobody else is doing," Ohsumi added. "In a way, that's what science is all about, and the joy of finding something inspires me."

Japanese scientist Yoshinori Ohsumi answers a phone call following a news that he won this year's Nobel Prize in medicine at his office in the Tokyo Institute of Technology campus in Yokohama, south of Tokyo, Monday, Oct. 3, 2016. Ohsumi was awarded this year's Nobel Prize in medicine on Monday, Oct. 3, for discoveries related to the degrading and recycling of cellular components. The Karolinska Institute honored Ohsumi for "brilliant experiments" in the 1990s on autophagy, the machinery with which cells recycle their content. Disrupted autophagy has been linked to various diseases including Parkinson's, diabetes and cancer, the institute said. (Junko Ozaki/Kyodo News via AP)

Nobel committee secretary Thomas Perlmann said Ohsumi seemed surprised when he was informed he had won the Nobel Prize.

"The first thing he said was 'ahhh.' He was very, very pleased," Perlmann said.

Nobel judges often award discoveries made decades ago, to make sure they have stood the test of time.

The term autophagy was coined in 1963 by Belgian scientist Christian de Duve, who shared the 1974 Nobel Prize in medicine for discoveries on cell structure and organization.

But before Ohsumi's research, scientists "didn't know what it did, they didn't know how it was controlled and they didn't know what it was relevant for," said David Rubinsztein, deputy director of the Institute for Medical Research at the University of Cambridge.

Now "we know that autophagy is important for a host of important mammalian functions." For example, it protects against starvation in the period when a newborn animal hasn't yet started breastfeeding, by providing energy, he said.

Japanese scientist Yoshinori Ohsumi scratches his head as he reacts photographers' request to smile following a news that he won this year's Nobel Prize in medicine at the Tokyo Institute of Technology campus in Yokohama, south of Tokyo, Monday, Oct. 3, 2016. Ohsumi was awarded this year's Nobel Prize in medicine on Monday, Oct. 3, for discoveries related to the degrading and recycling of cellular components. (Junko Ozaki/Kyodo News via AP)

It also removes proteins that clump together abnormally in brain cells, which is important in conditions like Huntington's and Parkinson's diseases and some forms of dementia. If autophagy didn't do that job, "the diseases would appear more early and be more aggressive," he said.

Animal studies suggest that boosting autophagy can ease and delay such diseases, said Rubinsztein, whose lab is pursuing that approach for therapy.

"As time goes on, people are finding connections with more and more diseases" and normal cellular operations, he said.

The fundamental significance of autophagy was only recognized after Ohsumi's "paradigm-shifting research" on yeast in the 1990s, the Nobel committee said. It said he published his "seminal discovery" of 15 genes crucial to autophagy in 1993, and cloned several of those genes in yeast and mammalian cells in subsequent studies.

"He actually unraveled which are the components which actually perform this whole process," Rune Toftgard, chairman of the Nobel Assembly, said.

Deficiencies in autophagy are linked to diseases associated with aging like Alzheimer's and Parkinson's, as well as with Type 2 diabetes, Toftgard said. Researchers are now trying to find out whether such diseases can be fought by boosting or suppressing the process.

"There are now over 40 to 50 clinical trials ongoing internationally to test different inhibitors or activators of autophagy," he said.

In Tokyo, Ohsumi said many details of autophagy are yet to be understood and that he hoped younger scientists would join him in looking for the answers.

"There is no finish line for science. When I find an answer to one question, another question comes up. I have never thought I have solved all the questions," he said. "So I have to keep asking questions to yeast."

It was the 107th award in the medicine category since the first Nobel Prizes were handed out in 1905.

Last year's prize was shared by three scientists who developed treatments for malaria and other tropical diseases.

The announcements continue with physics on Tuesday, chemistry on Wednesday and the Nobel Peace Prize on Friday. The economics and literature awards will be announced next week.

A photo of Nobel Prize for Medicine winner Yoshinori Ohsumi of Japan, is displayed on a screen at the Nobel Forum in Stockholm, Sweden, during the announcement of the Nobel Prize for Medicine, Monday Oct. 3, 2016. (Stina Stjernkvist / TT via AP)

Each prize is worth 8 million kronor ($930,000). The awards will be handed out at prize ceremonies in Stockholm and Oslo on Dec. 10, the anniversary of prize founder Alfred Nobel's death in 1896.

Nobel medicine prize: A look at the winner and his research

Yoshinori Ohsumi, a 71-year-old Japanese scientist and professor at the Tokyo Institute of Technology, is this year's winner of the Nobel Prize in medicine.

Here's a look at why he won and the significance of his discoveries:

OHSUMI'S RESEARCH

In this July, 2016 photo, Japanese scientist Yoshinori Ohsumi smiles at the Tokyo Institute of Technology campus in Yokohama, south of Tokyo. Ohsumi was awarded this year's Nobel Prize in medicine on Monday, Oct. 3, for discoveries related to the degrading and recycling of cellular components. The Karolinska Institute honored Ohsumi for "brilliant experiments" in the 1990s on autophagy, the machinery with which cells recycle their content. Disrupted autophagy has been linked to various diseases including Parkinson's, diabetes and cancer, the institute said. (Akiko Matsushita/Kyodo News via AP)

Ohsumi is being recognized for groundbreaking experiments in the 1990s dealing with autophagy, the "self-eating" process that lets a cell break down and recycle some of its contents, which rapidly provides fuel and building blocks.

Breakdowns in the autophagy process have been linked to a number of grave diseases including Parkinson's, diabetes and cancer.

The Karolinska Institute said researchers had known about autophagy (aw-TAH'-fuh-jee) for half a century, but its wide-ranging significance was only made clear by Ohsumi's experiments.

___

WHY NOW?

It is common for Nobel judges to honor people for discoveries that were actually made years or decades earlier to assure that the research was valid and its importance borne out over time.

In this file photo dated Friday, April 17, 2015, a national library employee shows the gold Nobel Prize medal awarded to the late novelist Gabriel Garcia Marquez, in Bogota, Colombia. There is no bigger international honor than the Nobel Prize, created by 19th-century Swedish industrialist Alfred Nobel, and the 2016 laureates will be named over the coming days to join the pantheon of greats who were honored in years gone by. (AP Photo/Fernando Vergara, FILE)

It may take many years before the relevance and value of some discoveries becomes clear.

___

SIGNIFICANCE

The Karolinska Institute said there is a surge in research about how to develop drugs that can target autophagy for the treatment of cell problems involved in many serious diseases.

Because of Ohsumi's research, and the experiments of those guided by it, the role of autophagy in controlling vital physiological functions is better understood and may be put to therapeutic use.

Japanese scientist Yoshinori Ohsumi smiles as he answers a reporter's question after learning that he won this year's Nobel Prize in medicine at the Tokyo Institute of Technology campus in Yokohama, south of Tokyo, Monday, Oct. 3, 2016. Ohsumi was awarded this year's Nobel Prize in medicine on Monday, Oct. 3, for discoveries related to the degrading and recycling of cellular components. The Karolinska Institute honored Ohsumi for "brilliant experiments" in the 1990s on autophagy, the machinery with which cells recycle their content. Disrupted autophagy has been linked to various diseases including Parkinson's, diabetes and cancer, the institute said. (Junko Ozaki/Kyodo News via AP)

REACTION

Ohsumi's initial response to winning a Nobel was sheer delight.

Nobel secretary Thomas Perlmann, who conveyed the news that he had won to the scientist, said that "the first thing he said was 'ahhh.' He was very, very pleased."

Later Ohsumi told Japanese broadcaster NHK that "as a scientist, I'm extremely honored." Speaking Japanese, he said he had wanted to pursue "something different from other people" when he decided to focus on autophagy.

Japanese scientist Yoshinori Ohsumi smiles in front of a sign congratulating him for winning this year's Nobel Prize in medicine at the Tokyo Institute of Technology campus in Yokohama, south of Tokyo, Monday, Oct. 3, 2016. Ohsumi was awarded this year's Nobel Prize in medicine on Monday, Oct. 3, for discoveries related to the degrading and recycling of cellular components. The Karolinska Institute honored Ohsumi for "brilliant experiments" in the 1990s on autophagy, the machinery with which cells recycle their content. Disrupted autophagy has been linked to various diseases including Parkinson's, diabetes and cancer, the institute said. (Junko Ozaki/Kyodo News via AP)

More information: www.nobelprize.org/nobel_prizes/medicine/laureates/2016/press.html 

http://medicalxpress.com/news/2016-10-yoshinori-ohsumi-japan-nobel-medicine.html