一項(xiàng)針對(duì)腦脊液蛋白與阿爾茨海默病相關(guān)的臨床癥狀與認(rèn)知正常的老年患者之間的關(guān)系的研究表明：β-淀粉樣蛋白相關(guān)的臨床病理的下降與P-tau蛋白磷酸化的tau蛋白升高有聯(lián)系,，相關(guān)研究論文發(fā)表在Archives of Neurology雜志上,。
加州圣地亞哥醫(yī)學(xué)院的大學(xué)Rahul S. Desikan醫(yī)學(xué)博士和同事評(píng)估了107阿爾茨海默氏病患者個(gè)體。他們檢查腦脊液（CSF）的tau蛋白181的磷酸化（P-tau蛋白181p）和腦脊液Αβ1-42的水平,。
結(jié)果表明腦脊液Αβ1-42的減少與腦脊液P-tau蛋白181p的升高之間有顯著聯(lián)系,。
這些研究發(fā)現(xiàn)與以前的研究結(jié)果相一致,，我們的結(jié)果表明臨床上正常的老年個(gè)體本身Αβ沉積并不與臨床病理特征下降有關(guān),，P-tau蛋白的存在是Αβ沉積以及臨床病理加速下降的關(guān)鍵環(huán)節(jié),。此外，我們的研究結(jié)果表明P-tau蛋白可以作為AD疾病相關(guān)退化的重要標(biāo)志,。
研究人員指出,，早期干預(yù)試驗(yàn)應(yīng)考慮腦脊液P-tau蛋白181p和腦脊液Αβ的1-42在患者體內(nèi)的情況。這項(xiàng)研究由來自美國國立衛(wèi)生研究院的資助青年學(xué)者獎(jiǎng),、阿爾茨海默氏病影像學(xué)和阿爾茨海默氏癥協(xié)會(huì)資助。（生物谷：Bioon.com）
doi:10.1001/archneurol.2011.3354
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Amyloid-β–Associated Clinical Decline Occurs Only in the Presence of Elevated P-tau
Rahul S. Desikan, MD, PhD; Linda K. McEvoy, PhD; Wesley K. Thompson, PhD; Dominic Holland, PhD; James B. Brewer, MD, PhD; Paul S. Aisen, MD; Reisa A. Sperling, MD; Anders M. Dale, PhD; for the Alzheimer's Disease Neuroimaging Initiative
Objective To elucidate the relationship between the 2 hallmark proteins of Alzheimer disease (AD), amyloid-β (Aβ) and tau, and clinical decline over time among cognitively normal older individuals.
Design A longitudinal cohort of clinically and cognitively normal older individuals assessed with baseline lumbar puncture and longitudinal clinical assessments.
Setting Research centers across the United States and Canada.
Patients: We examined 107 participants with a Clinical Dementia Rating (CDR) of 0 at baseline examination.
Main Outcome Measures Using linear mixed effects models, we investigated the relationship between cerebrospinal fluid (CSF) phospho-tau 181 (p-tau181p), CSF Aβ1-42, and clinical decline as assessed using longitudinal change in global CDR, CDR–Sum of Boxes, and the Alzheimer Disease Assessment Scale–cognitive subscale.
Results We found a significant relationship between decreased CSF Aβ1-42 and longitudinal change in global CDR, CDR–Sum of Boxes, and Alzheimer Disease Assessment Scale–cognitive subscale in individuals with elevated CSF p-tau181p. In the absence of CSF p-tau181p, the effect of CSF Aβ1-42 on longitudinal clinical decline was not significantly different from 0.
Conclusions In cognitively normal older individuals, Aβ-associated clinical decline during a mean of 3 years may occur only in the presence of ongoing downstream neurodegeneration.
