797 research outputs found
Preserved visuoconstruction in patients with Alzheimer's pathology and anti-neural autoantibodies: A case control study
BackgroundAlzheimer's disease (AD) is seldom reported to be associated with neural autoantibodies apart from those involved in axonal neurodegeneration and amyloidopathy in prior studies. Nevertheless, this is an under-investigated aspect of AD. As we do not know whether additional screening for autoantibodies in AD patients has additional diagnostic and therapeutic value, this study aims to shed light on whether visuoconstructive or figural memory capacities might distinguish these patient populations.MethodsIn this pilot case series, we investigated eight patients suffering from cognitive impairment associated with cerebrospinal fluid (CSF)-based Alzheimer pathology (AP) and with verified anti-neural autoantibodies (AP Aab+) compared to eight AD patients presenting no autoantibodies (Aab–) (AD Aab–). Patients files were reviewed retrospectively regarding their neuropsychological profile assessed via the CERAD (Consortium to Establish a Registry for Alzheimer's Disease) test battery and psychopathology measured by the AMDP (Manual for the Assessment and Documentation of Psychopathology in Psychiatry) system. We also relied on diagnostic parameters as in the CSF and magnetic resonance images.ResultsAll patients shared the same pattern of dysfunctional word-list learning and word-list recall resembling a hippocampus-dependent memory dysfunction. Furthermore, both patient groups revealed a CSF profile concurring with Alzheimer's disease. However, visuoconstructive capacity, but not figure recall was preserved in AP Aab+ patients, but not in AD Ab-patients with the shared hippocampus-based memory dysfunction. We observed no relevant differences between the AP Aab+ and AD Aab– groups in CSF cell-counts or intrathecal IgG synthesis. The relative frequency of hippocampal and focal atrophy did not differ either between AP Aab+ and AD Aab– groups.DiscussionOur pilot findings are encouraging us to conduct large-scale studies to replicate our discovery of preserved visuoconstruction in AP Aab+ patients with hippocampus-based memory dysfunction. The role of anti-neural autoantibodies is still not fully understood. The detection of these autoantibodies might imply another disease pathology that could be either neuroprotective or be affecting other brain regions, i.e., less pronounced disease activity in the right temporo-parietal regions mainly involved in visuoconstruction.</jats:sec
Cerebrospinal fluid biomarkers in psychiatric autoimmune encephalitis: a retrospective cohort study
Background: Psychiatric autoimmune encephalitis (pAE) is a growing field of interest in diagnosis and therapy in psychiatric hospitals and institutions. This study investigates the relevant extent to which there are potential biomarkers in cerebrospinal fluid (CSF) that can differentiate against a cohort with neurodegenerative disease.
Methods: We included in this study a total of 27 patients with possible and definite psychiatric autoimmune encephalitis and compared with a cohort with CSF-based AD (n = 27) different biomarkers in CSF such as lactate, cell count, % lymphocytes, % monocytes, total protein content, albumin, immunoglobulins G (IgG), M (IgM) and A (IgA), CSF/serum albumin ratio, CSF/serum IgG ratio, CSF/serum IgA ratio, intrathecal IgG synthesis, blood–brain barrier disruption, specific antibody synthesis for measles, rubella, herpes simplex virus, varicella zoster virus, Ebstein-Barr virus and cytomegalovirus, total tau protein (t-tau), phosphorylated tau protein 181 (p-tau181), amyloid beta 42 (Aß42), amyloid beta 40 (Aß40) and the amyloid beta 42/ amyloid beta 40 (Aß42/40) ratio.
Results: The p-tau 181 was elevated above cut-off values in both possible pAE and AD. However, in definitive pAE, p-tau181 levels were not elevated. When elevated p-tau181 levels in possible AE were compared with those in AD, we found relevant differences, such as a relative increase in p-tau181 in AD patients. Elevated p-tau181 levels were detected in possible psychiatric AEs with IgLON5, glycine, recoverin, titin, and nonspecific neuropil antibodies in serum and IgLON5, titin, Yo, and nonspecific neuropil autoantibodies in CSF. In addition, we detected elevated levels of p-tau181 and IgLON5 autoantibodies in serum and CSF, and Yo autoantibodies in CSF in patients with definitive pAE. Interestingly, we observed a higher CSF/serum IgM ratio in possible and definitive pAE than in AD patients.
Conclusion: Our results suggest that neuroaxonal brain damage may occur in specific psychiatric AEs associated with IgLON5, glycine, recoverin, and titin autoantibodies. Further research should focus on the CSF/serum IgM ratio as an early marker of autoantibody production in pAE compared to AD as a potential biomarker for differential diagnosis.Open-Access-Publikationsfonds 202
Biomarkers of neurodegeneration in neural autoantibody-associated psychiatric syndromes: A retrospective cohort study
BACKGROUND: 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. METHODS: 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. RESULTS: 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. DISCUSSION: 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
Longitudinally persisting KCNA2-autoantibodies in mild amnestic dementia with Alzheimer´s pathology – Report and literature review
Case report: Mixed dementia associated with autoantibodies targeting the vesicular glutamate transporter 2
BACKGROUND: Autoantibodies against the vesicular glutamate transporter type 2 (VGlut2) can trigger impaired synaptic signaling and are described here for the first time in association with mixed dementia. METHODS: We report on a 71-year-old female patient with a dementing syndrome who underwent a thorough dementia diagnosis including neuropsychological testing, magnetic resonance imaging (MRI), 18F-fluorodesoxyglucose positron emission tomography (FDG-PET), and a spinal tap to search for neural autoantibodies. RESULTS: Our patient exhibited mixed dementia. Her CSF revealed elevated ptau 181 protein and a reduced Aß42/40 ratio indicating Alzheimer's disease (AD) pathology. In addition, neuropsychological testing showed a profile consistent with AD with impaired memory, reduced semantic word fluency, naming disorder, and impaired visuoconstructive skills. Nevertheless, in-depth neuropsychological testing also revealed marked psychomotor slowing and visuospatial perceptual impairments that are more indicative of the presence of DLB. Overall, her dementia is more likely of mixed pathology. In addition, we repeatedly detected VGlut2 autoantibodies in her serum.
CONCLUSION: To the best of our knowledge, this report is the first to describe mixed dementia associated with VGlut2 autoantibodies
Acute neuronal cell death and neuroinflammation per se do not trigger secondary autoimmune encephalitis
Bianca Garavelli studiosa e scrittrice
Bianca Garavelli (Vigevano, 1958-2021) was a highly regarded figure in the literary world, both on the critical and creative side. Author of important critical studies on Dante and of a successful commentary on the Commediam (begun under the supervision of Maria Corti but then continued independently), as well as critic and reviewer for newspapers and periodicals, Garavelli also wrote and published poems, novels and short stories. This article offers an exhaustive bio-bibliographical profile of Bianca Garavelli, whose literary work in various fields is reconstructed and critically examined
Let´s (watch me) play : which factors relate to Let´s Play addiction?
Author Bianca Haun, BScZusammenfassungen in englischer SpracheMasterarbeit Universität Linz 201
Identifizierung DNA-komplexierter Granulocytenproteine als Zielantigene Colitis-ulcerosa-assoziierter Antikörper
KCNA2 IgG autoimmunity in neuropsychiatric diseases
http://dx.doi.org/10.13039/501100001674 Fondation Leducqhttp://dx.doi.org/10.13039/501100002347 Bundesministerium für Bildung und Forschunghttp://dx.doi.org/10.13039/501100009318 Helmholtz Associationhttp://dx.doi.org/10.13039/100016021 Corona-Stiftunghttp://dx.doi.org/10.13039/501100001659 Deutsche Forschungsgemeinschafthttp://dx.doi.org/10.13039/501100000780 European Commissio
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