Juhl Aaron Levin, Grenzer Insa Maria, Teegen Bianca, Wiltfang Jens, Fitzner Dirk, Hansen Niels
Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
Translational Psychoneuroscience, Department of Psychiatry and Psychotherapy, University Medical Center Göttingen, Von-Siebold-Str. 5, 37075, Göttingen, Germany.
J Transl Autoimmun. 2022 Oct 5;5:100169. doi: 10.1016/j.jtauto.2022.100169. eCollection 2022.
Autoantibody-associated psychiatric syndromes are a novel disease entity that is not fully understood. Several lines of evidence suggest that neurodegenerative processes are involved here. We are investigating whether autoantibody-positive psychiatric syndromes differ from those that are autoantibody-negative in cerebrospinal fluid (CSF) neurodegeneration markers.
We retrospectively analyzed data from 167 psychiatric patients at the University Medical Center Göttingen from 2017 to 2020. We divided this patient cohort into two, namely antibody-positive and antibody-negative. We compared various clinical features, neurodegeneration markers, and their autoantibody status in CSF and serum. We then compared both cohorts' neurodegeneration markers to a representative Alzheimer cohort. We subdivided the patients into their diverse psychiatric syndromes according to the manual to assess and document psychopathology in psychiatry (the AMDP), and compared the neurodegeneration markers.
Antibody-associated psychiatric syndromes do not appear to reveal significantly greater neurodegeneration than their antibody-negative psychiatric syndromes. 71% of antibody-positive patients fulfilled the criteria for a possible and 22% for a definitive autoimmune encephalitis. Our autoantibody-positive patient cohort's relative risk to develop an possible autoimmune encephalitis was 9%. We also noted that phosphorylated tau protein 181 (ptau 181) did not significantly differ between antibody-associated psychiatric syndromes and our Alzheimer cohort. The psycho-organic syndrome usually exhibits the most prominent neurodegeneration markers, both in antibody-positive and antibody-negative psychiatric patients.
We did not find hints for neurodegenerative processes in our antibody-positive versus AD cohort considering total tau or amyloid markers. However, our findings indicate that the neurodegeneration marker ptau181 does not differ significantly between antibody-positive and Alzheimer cohorts, further suggesting axonal neurodegeneration in antibody-positive patients as AD patients have an elevated ptau181. The evidence we uncovered thus suggests that axonal neurodegeneration might affect patients suffering from autoantibody-associated psychiatric syndromes.
自身抗体相关的精神综合征是一种尚未完全被理解的新型疾病实体。多项证据表明，神经退行性过程与此有关。我们正在研究自身抗体阳性的精神综合征在脑脊液（CSF）神经退行性变标志物方面是否与自身抗体阴性的精神综合征有所不同。
我们回顾性分析了2017年至2020年在哥廷根大学医学中心的167例精神科患者的数据。我们将这个患者队列分为两组，即抗体阳性组和抗体阴性组。我们比较了各种临床特征、神经退行性变标志物以及它们在脑脊液和血清中的自身抗体状态。然后，我们将两组的神经退行性变标志物与一个有代表性的阿尔茨海默病队列进行比较。我们根据《精神科精神病理学评估与记录手册》（AMDP）将患者细分为不同的精神综合征，并比较神经退行性变标志物。
与抗体阴性的精神综合征相比，抗体相关的精神综合征似乎并未显示出明显更严重的神经退行性变。71%的抗体阳性患者符合可能的自身免疫性脑炎标准，22%符合确诊的自身免疫性脑炎标准。我们自身抗体阳性患者队列发生可能的自身免疫性脑炎的相对风险为9%。我们还注意到，在抗体相关精神综合征和我们的阿尔茨海默病队列之间，磷酸化tau蛋白181（ptau 181）没有显著差异。在抗体阳性和抗体阴性的精神科患者中，精神器质性综合征通常表现出最显著的神经退行性变标志物。
在考虑总tau或淀粉样蛋白标志物时，我们在抗体阳性与阿尔茨海默病队列中未发现神经退行性过程的迹象。然而，我们的研究结果表明，抗体阳性组和阿尔茨海默病队列之间的神经退行性变标志物ptau181没有显著差异，这进一步表明抗体阳性患者存在轴突神经退行性变，因为阿尔茨海默病患者的ptau181升高。因此，我们发现的证据表明轴突神经退行性变可能影响自身抗体相关精神综合征患者。
