알츠하이며, REST(RE1-Silencing Transcription) 단백질과 관련이 있다.
알츠하이머가 ‘REST’라 불리는 단백질과 관련있다는 연구결과가 나왔다.
뉴욕타임스(NYT)가 금년 3월19일(현지시간) 보도한 것이다.
미국 하버드대학 브루스 얜크너 교수 연구팀은 이날 네이처지에 발표한 논문에서
태아의 뇌에서 주로 작용하는 것으로 알려진 REST 단백질이
노인의 뉴런(신경세포)을 노화와 관련된 스트레스로부터 지켜주는 것으로 보인다고 주장했다.
조사결과 73∼106세 건강한 노년층의 뇌에서는 이 단백질이 많이 발견됐지만
알츠하이머나 다른 종류의 치매를 앓는 이의 뇌 주요부분에서는 이 단백질이 급격히 고갈된 것으로 나타났다.
연구진은 이 단백질의 감소가 뇌기능을 저하시킨 원인인지, 아니면 뇌기능 저하로 인한 결과인지는
아직 단언할 수 없다며 후속 연구가 필요하다고 덧붙였다.
알츠하이머 관련 권위자인 MIT대학 피코어연구소 리후에이 차이 교수는 “이번 연구는
왜 어떤 사람은 다른 이보다 알츠하이머에 더 취약한 지를 설명하는 출발점이 될 수 있다”고 평가했다.
- “알츠하이머, ‘REST’ 단백질과 관련 있다”<하버드대> (서울=연합뉴스) 나확진 기자 -
원문과 관련된 자료를 소개하는 바 이같은 논문의 핵심은 장차 알츠하이머 치료에 깊이 개입될 것이기 때문이다.
Protein May Hold the Key to Who Gets Alzheimer’s
By PAM BELLUCKMARCH 19, 2014 New York Times
It is one of the big scientific mysteries of Alzheimer’s disease: Why do some people whose brains
accumulate the plaques and tangles so strongly associated with Alzheimer’s not develop the disease?
Now, a series of studies by Harvard scientists suggests a possible answer, one that could lead to new treatments if confirmed by other research.
The memory and thinking problems of Alzheimer’s disease and other dementias, which affect an
estimated seven million Americans, may be related to a failure in the brain’s stress response system,
the new research suggests. If this system is working well, it can protect the brain from abnormal
Alzheimer’s proteins; if it gets derailed, critical areas of the brain start degenerating.
“This is an extremely important study,” said Li-Huei Tsai, director of the Picower Institute for Learning
and Memory at the Massachusetts Institute of Technology, who was not involved in the research but
wrote a commentary accompanying the study. “This is the first study that is really starting to provide
a plausible pathway to explain why some people are more vulnerable to Alzheimer’s than other people.”
Photo
The research, published on Wednesday in the journal Nature, focuses on a protein previously thought to act mostly in the brains of developing fetuses. The scientists found that the protein also appears to protect neurons in healthy older people from aging-related stresses. But in people with Alzheimer’s and other dementias, the protein is sharply depleted in key brain regions.
Experts said if other scientists could replicate and expand upon the findings, the role of the protein, called REST, could spur development of new drugs for dementia, which has so far been virtually impossible to treat. But they cautioned that much more needed to be determined, including whether the decline of REST was a cause, or an effect, of brain deterioration, and whether it was specific enough to neurological diseases that it could lead to effective therapies.
Continue reading the main story
“You’re going to see a lot of papers now following up on it,” said Dr. Eric M. Reiman, executive director of the Banner Alzheimer’s Institute in Phoenix, who was not involved in the study. “While it’s a preliminary finding, it raises an avenue that hasn’t been considered before. And if this provides a handle on which to understand normal brain aging, that will be great, too.”
REST, a regulator that switches off certain genes, is primarily known to keep fetal neurons in an immature state until they develop to perform brain functions, said Dr. Bruce A. Yankner, a professor of genetics at Harvard Medical School and the lead author of the new study. By the time babies are born, REST becomes inactive, he said, except in some areas outside the brain like the colon, where it seems to suppress cancer.
While investigating how different genes in the brain change as people age, Dr. Yankner’s team was startled to find that REST was the most active gene regulator in older brains.
“Why should a fetal gene be coming on in an aging brain?” he wondered. He hypothesized that it was because in aging, as in birth, brains encounter great stress, threatening neurons that cannot regenerate if harmed.
His team discovered that REST appears to switch off genes that promote cell death, protecting neurons from normal aging processes like energy decrease, inflammation and oxidative stress.
출처:
http://www.brainleadersandlearners.com/ellen-weber/stress-masks-as-savior-to-strike-as-killer/
REST protein 저하가 단독적으로 작용되는 원인으로 인정하는 학자는 없다.
Alzhiemer's Disease의 유발인자는 결코 한 두가지로 한정된 것이 아니다.
다만 태아의 뇌에 REST가 풍부한 것이 어디로 어떻게 파괴되었는지 알아야 한다는 것은 의미가 크다.
상기 내용에서 확인된 바 같은 노령에서 AD를 일으킬 요소가 있음에도 REST leve 여하에 따라
낮은 사람에게 집중적으로 AD 발생빈도가 높다는 점에서 치료수단을 개발하는 대 기여도가 클 것이다.
모든 인체의 분자들이 그렇듯 REST 역시 Colon Cancer를 억제하는 것으로 보인다는 사실은
흥미있는 것이며, Brain Response System의 작동이 실패했을 때 관계되는 것은
REST 뿐 아니라 Addiction과 관계가 있다는 사실은 부수적으로 얻게 되는 또 하나의 소득이기도 하다.
위 그림에서 Brain Response System에서 알려진 것 외 또 다른 사실도 그렇다.
Addition에 대한 개념이 달라진다는 것이다. Reward System에 의한 경로외에
Brain Response System의 작동 결함으로 유발되는 두 개의 신경전달물질,
Amygdala에서 나오는 CRF(Corticotropic Releasing Factor)와 Basal Ganglia에서 나오는
Dyporphine-k Opioid System에 의해
Addiction은 즐거운 기분을 위해서가 아니라 반복되는 금단에 따르는 불안, 공포, 불쾌감 등의 현상을 피하기 위해
중독현상은 지속될 수 밖에 없다는 것이다.
이것은 정서적 고통을 유발하는 neurobiology 상의 이해수준을 높여 준 결과이자
동시에 멋진 중독치료의 방안을 제안하는 것이기에 결코 간과할 수 없는 연구과제를 남긴다.
연구 발전에 모든 과학자들이 집중하는 이유가 바로 AD이든 Addiction이든 이렇게 연결 얽혀있음에 대한
해답을 위한 집념, 그 결과에 대한 유혹에 있을 것이다.
참고 자료 및 출처;
http://blog.unhaggle.com/commuting-dangers/
http://www.brainleadersandlearn
http://alert.psychiatricnews.org/2013/11/brain-stress-systems-may-be-key-piece.htmlers.com/ellen-weber/stress-masks-as-savior-to-strike-as-killer/http://www.nytimes.com/2014/03/20/health/fetal-gene-may-protect-brain-from-alzheimers-study-finds.html?_r=0
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