近三十年來第一次修訂老年癡呆症診斷標準(圖)

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年癡呆症是一種不斷進化發展的慢性病,美國國立衛生研究所(NIH)對老年癡呆症的診斷標準進行了進幾十年來的首次修訂。新的診斷標準把老年癡呆症分為三個階段:1)臨床前期;2)輕度認知能力障礙;3)老年癡呆症。

新的診斷標準的應用有利於研究老年癡呆症的病因和病程,對新療法的開發亦有幫助。


健康人的大腦對比老年癡呆症人的大腦

Alzheimer’s diagnostic guidelines updated for first time in decades

For the first time in 27 years, clinical diagnostic criteria for Alzheimer’s disease dementia have been revised, and research guidelines for earlier stages of the disease have been characterized to reflect a deeper understanding of the disorder. The National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease outline some new approaches for clinicians and provide scientists with more advanced guidelines for moving forward with research on diagnosis and treatments. They mark a major change in how experts think about and study Alzheimer’s disease. Development of the new guidelines was led by the National Institutes of Health and the Alzheimer’s Association.

The original criteria were the first to address the disease and described only later stages, when symptoms of dementia are already evident. The updated guidelines announced today cover the full spectrum of the disease as it gradually changes over many years. They describe the earliest preclinical stages of the disease, mild cognitive impairment, and dementia due to Alzheimer’s pathology. Importantly, the guidelines now address the use of imaging and biomarkers in blood and spinal fluid that may help determine whether changes in the brain and those in body fluids are due to Alzheimer’s disease. Biomarkers are increasingly employed in the research setting to detect onset of the disease and to track progression, but cannot yet be used routinely in clinical diagnosis without further testing and validation.

“Alzheimer’s research has greatly evolved over the past quarter of a century. Bringing the diagnostic guidelines up to speed with those advances is both a necessary and rewarding effort that will benefit patients and accelerate the pace of research,” said National Institute on Aging Director Richard J. Hodes, M.D.

“We believe that the publication of these articles is a major milestone for the field,” said William Thies, Ph.D., chief medical and scientific officer at the Alzheimer’s Association. “Our vision is that this process will result in improved diagnosis and treatment of Alzheimer’s, and will drive research that ultimately will enable us to detect and treat the disease earlier and more effectively. This would allow more people to live full, rich lives without—or with a minimum of—Alzheimer’s symptoms.”

The new guidelines appear online April 19, 2011 in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association. They were developed by expert panels convened last year by the National Institute on Aging (NIA), part of the NIH, and the Alzheimer’s Association. Preliminary recommendations were announced at the Association’s International Conference on Alzheimer’s Disease in July 2010, followed by a comment period.

Guy M. McKhann, M.D., Johns Hopkins University School of Medicine, Baltimore, and David S. Knopman, M.D., Mayo Clinic, Rochester, Minn., co-chaired the panel that revised the 1984 clinical Alzheimer’s dementia criteria. Marilyn Albert, Ph.D., Johns Hopkins University School of Medicine, headed the panel refining the MCI criteria. Reisa A. Sperling, M.D., Brigham and Women’s Hospital, Harvard Medical School, Boston, led the panel tasked with defining the preclinical stage. The journal also includes a paper by Clifford Jack, M.D., Mayo Clinic, Rochester, Minn., as senior author, on the need for and concept behind the new guidelines.

The original 1984 clinical criteria for Alzheimer’s disease, reflecting the limited knowledge of the day, defined Alzheimer’s as having a single stage, dementia, and based diagnosis solely on clinical symptoms. It assumed that people free of dementia symptoms were disease-free. Diagnosis was confirmed only at autopsy, when the hallmarks of the disease, abnormal amounts of amyloid proteins forming plaques and tau proteins forming tangles, were found in the brain.

Since then, research has determined that Alzheimer’s may cause changes in the brain a decade or more before symptoms appear and that symptoms do not always directly relate to abnormal changes in the brain caused by Alzheimer’s. For example, some older people are found to have abnormal levels of amyloid plaques in the brain at autopsy yet never showed signs of dementia during life. It also appears that amyloid deposits begin early in the disease process but that tangle formation and loss of neurons occur later and may accelerate just before clinical symptoms appear.

To reflect what has been learned, the National Institute on Aging/Alzheimer’s Association Diagnostic Guidelines for Alzheimer’s Disease cover three distinct stages of Alzheimer’s disease:

  • Preclinical – The preclinical stage, for which the guidelines only apply in a research setting, describes a phase in which brain changes, including amyloid buildup and other early nerve cell changes, may already be in process. At this point, significant clinical symptoms are not yet evident. In some people, amyloid buildup can be detected with positron emission tomography (PET) scans and cerebrospinal fluid (CSF) analysis, but it is unknown what the risk for progression to Alzheimer’s dementia is for these individuals. However, use of these imaging and biomarker tests at this stage are recommended only for research. These biomarkers are still being developed and standardized and are not ready for use by clinicians in general practice.
  • Mild Cognitive Impairment (MCI) – The guidelines for the MCI stage are also largely for research, although they clarify existing guidelines for MCI for use in a clinical setting. The MCI stage is marked by symptoms of memory problems, enough to be noticed and measured, but not compromising a person’s independence. People with MCI may or may not progress to Alzheimer’s dementia. Researchers will particularly focus on standardizing biomarkers for amyloid and for other possible signs of injury to the brain. Currently, biomarkers include elevated levels of tau or decreased levels of beta-amyloid in the CSF, reduced glucose uptake in the brain as determined by PET, and atrophy of certain areas of the brain as seen with structural magnetic resonance imaging (MRI). These tests will be used primarily by researchers, but may be applied in specialized clinical settings to supplement standard clinical tests to help determine possible causes of MCI symptoms.
  • Alzheimer’s Dementia – These criteria apply to the final stage of the disease, and are most relevant for doctors and patients. They outline ways clinicians should approach evaluating causes and progression of cognitive decline. The guidelines also expand the concept of Alzheimer’s dementia beyond memory loss as its most central characteristic. A decline in other aspects of cognition, such as word-finding, vision/spatial issues, and impaired reasoning or judgment may be the first symptom to be noticed. At this stage, biomarker test results may be used in some cases to increase or decrease the level of certainty about a diagnosis of Alzheimer’s dementia and to distinguish Alzheimer’s dementia from other dementias, even as the validity of such tests is still under study for application and value in everyday clinical practice.

The panels purposefully left the guidelines flexible to allow for changes that could come from emerging technologies and advances in understanding of biomarkers and the disease process itself.

“The guidelines discuss biomarkers currently known, and mention others that may have future applications,” said Creighton H. Phelps, Ph.D., of the NIA Alzheimer’s Disease Centers Program. “With researchers worldwide striving to develop, validate and standardize the application of biomarkers at every stage of Alzheimer’s disease, we devised a framework flexible enough to incorporate new findings.”

http://www.nia.nih.gov/NewsAndEvents/PressReleases/PR20110419guidelines.htm



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  • 所有跟帖: 

    謝謝.人人想長壽,但又怕老年癡呆症.這病到目前為止都無法治療.有什麽可防止的措施嗎? -swj2000- 給 swj2000 發送悄悄話 swj2000 的博客首頁 (115 bytes) () 04/19/2011 postreply 21:30:32

    生命在於活動和壓力,如果鐵娘子撒切爾夫人 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (105 bytes) () 04/19/2011 postreply 21:41:14

    老中醫也很少有老年癡呆,愈老愈忙咧。 -ooopsss- 給 ooopsss 發送悄悄話 ooopsss 的博客首頁 (0 bytes) () 04/19/2011 postreply 21:50:54

    此話不假,看過一個紀錄片說北京郊區有一個 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (69 bytes) () 04/19/2011 postreply 21:59:06

    據說她有特異功能,愈人無數。 -ooopsss- 給 ooopsss 發送悄悄話 ooopsss 的博客首頁 (0 bytes) () 04/19/2011 postreply 22:12:36

    忘了她的姓名,鄧小平為她造了一幢樓,並封她為院長。。。 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (49 bytes) () 04/19/2011 postreply 22:29:22

    你說的大概是雙橋老太太羅有明 -dudaan- 給 dudaan 發送悄悄話 dudaan 的博客首頁 (0 bytes) () 04/20/2011 postreply 05:24:35

    就是她!謝謝!羅有明,女,1904年生人。從小學習祖傳中醫,中國正骨名醫, -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (197 bytes) () 04/20/2011 postreply 14:59:10

    介個現象有意思。老中醫裏確實沒有“老年癡呆症”。 -qiuqiu04.- 給 qiuqiu04. 發送悄悄話 (25 bytes) () 04/22/2011 postreply 20:34:17

    多用腦勤鍛煉有助於預防老年癡呆,可諾貝爾獎得主高錕也勤用腦,勤鍛煉,還是老年癡呆。 -swj2000- 給 swj2000 發送悄悄話 swj2000 的博客首頁 (71 bytes) () 04/19/2011 postreply 22:24:55

    還有基因的作用。幾乎所有的慢性病 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (37 bytes) () 04/19/2011 postreply 22:33:12

    期待用基因療法治老年癡呆症有突破性進展。 -ooopsss- 給 ooopsss 發送悄悄話 ooopsss 的博客首頁 (0 bytes) () 04/19/2011 postreply 23:11:01

    同意這個! -jck6- 給 jck6 發送悄悄話 jck6 的博客首頁 (0 bytes) () 04/20/2011 postreply 07:15:39

    同意。基因加環境因素的綜合結果 -jck6- 給 jck6 發送悄悄話 jck6 的博客首頁 (0 bytes) () 04/20/2011 postreply 07:21:31

    說的是! -swj2000- 給 swj2000 發送悄悄話 swj2000 的博客首頁 (0 bytes) () 04/20/2011 postreply 11:51:46

    除了多用腦勤鍛煉,健康、營養的飲食也很重要。佛教認為,殺生多易得愚癡及投生畜生道。 -ooopsss- 給 ooopsss 發送悄悄話 ooopsss 的博客首頁 (0 bytes) () 04/19/2011 postreply 22:49:14

    據分析高錕是遺傳,其父也是70開始老年癡呆。 -pisces-hk- 給 pisces-hk 發送悄悄話 pisces-hk 的博客首頁 (0 bytes) () 04/20/2011 postreply 07:47:34

    老年癡呆症不是病,是人該死沒死成的悲哀?自殺/被殺是治療的最好方法? -劈劈啪啪- 給 劈劈啪啪 發送悄悄話 (0 bytes) () 04/20/2011 postreply 09:55:19

    有趣的說法。其實現代醫學還是治標不治本,導致 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (234 bytes) () 04/20/2011 postreply 14:55:55

    回複:個人的看法是現代醫學的基因治療和幹細胞療法不但可以治療疾病而且將從根本上解決疾病產生的原因。 -幹細胞之友- 給 幹細胞之友 發送悄悄話 (4132 bytes) () 04/20/2011 postreply 15:50:35

    幹細胞和基因療法談得多,離開臨床應用尚遠。小布什時代,美國保守派還反對幹細胞研究。 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (41 bytes) () 04/20/2011 postreply 17:26:41

    幹細胞研究與應用的倫理思考(胡慶澧 丘祥興 沈銘賢 《中國醫學倫理學》 2010年03期):幹細胞研究與應用 -JoshuaChow- 給 JoshuaChow 發送悄悄話 JoshuaChow 的博客首頁 (237 bytes) () 04/20/2011 postreply 17:36:09

    回複:幹細胞和基因療法談得多,離開臨床應用尚遠。小布什時代,美國保守派還反對幹細胞研究。 -幹細胞之友- 給 幹細胞之友 發送悄悄話 (15775 bytes) () 04/20/2011 postreply 19:19:57

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