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2. A quantitative Lewy-fold-specific alpha-synuclein seed amplification assay as a progression marker for Parkinson’s disease

Author

Bernhardt, Alexander M., Longen, Sebastian, Trossbach, Svenja V., Rossi, Marcello, Weckbecker, Daniel, Schmidt, Felix, Jäck, Alexander, Katzdobler, Sabrina, Fietzek, Urban M., Weidinger, Endy, Palleis, Carla, Ruf, Viktoria, Baiardi, Simone, Parchi, Piero, Höglinger, Günter U., Matthias, Torsten, Levin, Johannes, and Giese, Armin

Published
2025
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15. Correction to: 4-Repeat tau seeds and templating subtypes as brain and CSF biomarkers of frontotemporal lobar degeneration

Author

Saijo, Eri, Metrick, Michael A, Koga, Shunsuke, Parchi, Piero, Litvan, Irene, Spina, Salvatore, Boxer, Adam, Rojas, Julio C, Galasko, Douglas, Kraus, Allison, Rossi, Marcello, Newell, Kathy, Zanusso, Gianluigi, Grinberg, Lea T, Seeley, William W, Ghetti, Bernardino, Dickson, Dennis W, and Caughey, Byron

Subjects
Biomedical and Clinical Sciences, Neurosciences, Neurodegenerative, Dementia, Frontotemporal Dementia (FTD), Alzheimer's Disease Related Dementias (ADRD), Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Rare Diseases, Brain Disorders, Acquired Cognitive Impairment, Aging, Neurological, Clinical Sciences, Neurology & Neurosurgery
Abstract

The original version of this article unfortunately contained a mistake. The Panel A in the published figure 5 is incorrect. The corrected Figure 5 is placed in the following page.

Published
2020

16. 4-Repeat tau seeds and templating subtypes as brain and CSF biomarkers of frontotemporal lobar degeneration

Author

Saijo, Eri, Metrick, Michael A, Koga, Shunsuke, Parchi, Piero, Litvan, Irene, Spina, Salvatore, Boxer, Adam, Rojas, Julio C, Galasko, Douglas, Kraus, Allison, Rossi, Marcello, Newell, Kathy, Zanusso, Gianluigi, Grinberg, Lea T, Seeley, William W, Ghetti, Bernardino, Dickson, Dennis W, and Caughey, Byron

Subjects
Biomedical and Clinical Sciences, Neurosciences, Dementia, Neurodegenerative, Frontotemporal Dementia (FTD), Alzheimer's Disease Related Dementias (ADRD), Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Rare Diseases, Alzheimer's Disease, Pick's Disease, Brain Disorders, Acquired Cognitive Impairment, Aging, 4.2 Evaluation of markers and technologies, 2.1 Biological and endogenous factors, Neurological, Biomarkers, Fluoroimmunoassay, Frontotemporal Lobar Degeneration, Humans, Protein Isoforms, Sensitivity and Specificity, tau Proteins, Tau, Progressive supranuclear palsy, Corticobasal degeneration, Strain, Diagnosis, Biomarker, Clinical Sciences, Neurology & Neurosurgery
Abstract

To address the need for more meaningful biomarkers of tauopathies, we have developed an ultrasensitive tau seed amplification assay (4R RT-QuIC) for the 4-repeat (4R) tau aggregates of progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), and other diseases with 4R tauopathy. The assay detected seeds in 106-109-fold dilutions of 4R tauopathy brain tissue but was orders of magnitude less responsive to brain with other types of tauopathy, such as from Alzheimer's disease cases. The analytical sensitivity for synthetic 4R tau fibrils was ~ 50 fM or 2 fg/sample. A novel dimension of this tau RT-QuIC testing was the identification of three disease-associated classes of 4R tau seeds; these classes were revealed by conformational variations in the in vitro amplified tau fibrils as detected by thioflavin T fluorescence amplitudes and FTIR spectroscopy. Tau seeds were detected in postmortem cerebrospinal fluid (CSF) from all neuropathologically confirmed PSP and CBD cases but not in controls. CSF from living subjects had weaker seeding activities; however, mean assay responses for cases clinically diagnosed as PSP and CBD/corticobasal syndrome were significantly higher than those from control cases. Altogether, 4R RT-QuIC provides a practical cell-free method of detecting and subtyping pathologic 4R tau aggregates as biomarkers.

Published
2020

17. Immune landscape of the enteric nervous system differentiates Parkinson's disease patients from controls: The PADUA-CESNE cohort

Author

Campagnolo, M, Weis, L, Sandre, M, Tushevski, A, Russo, F, Savarino, E, Carecchio, M, Stocco, E, Macchi, V, De Caro, R, Parchi, P, Bubacco, L, Porzionato, A, Antonini, A, Emmi, A, Campagnolo M., Weis L., Sandre M., Tushevski A., Russo F. P., Savarino E., Carecchio M., Stocco E., Macchi V., De Caro R., Parchi P., Bubacco L., Porzionato A., Antonini A., Emmi A., Campagnolo, M, Weis, L, Sandre, M, Tushevski, A, Russo, F, Savarino, E, Carecchio, M, Stocco, E, Macchi, V, De Caro, R, Parchi, P, Bubacco, L, Porzionato, A, Antonini, A, Emmi, A, Campagnolo M., Weis L., Sandre M., Tushevski A., Russo F. P., Savarino E., Carecchio M., Stocco E., Macchi V., De Caro R., Parchi P., Bubacco L., Porzionato A., Antonini A., and Emmi A.

Abstract

Background: Gastrointestinal dysfunction has emerged as a prominent early feature of Parkinson's Disease, shedding new light on the pivotal role of the enteric nervous system in its pathophysiology. However, the role of immune-cell clusters and inflammatory and glial markers in the gut pathogenetic process needs further elucidation. Objectives: We aimed to study duodenum tissue samples to characterize PD's enteric nervous system pathology further. Twenty patients with advanced PD, six with early PD, and 18 matched controls were included in the PADUA-CESNE cohort. Methods: Duodenal biopsies from 26 patients with early to advanced stage PD and 18 age-matched HCs were evaluated for the presence of surface markers (CD3+, CD4+, CD8+, CD20+, CD68+, HLA-DR), presence of misfolded alpha-synuclein and enteric glial alteration (GFAP). Correlation of immulogic pattern and clinical characteristic were analyzed. Results: The findings validate that in patients with Parkinson's Disease, the activation and reactive gliosis are linked to the neurodegeneration triggered by the presence of misfolded alpha-synuclein in the enteric nervous system. This process intensifies from the initial to the advanced stages of the disease. The clusters of T- and B-lymphocytes in the enteric system, along with the overall expression of HLA-DR in antigen-presenting cells, exceeded those in the control group. Conversely, no differences in terms of macrophage populations were found. Conclusions: These findings broaden our understanding of the mechanisms underlying the enteric nervous system's involvement in PD and point to the gastrointestinal system as a potential therapeutic target, especially in the early stages of the disease. Moreover, our results propose a role of T- and B-lymphocytes in maintaining inflammation and ultimately influencing alpha-synuclein misfolding and aggregation.

Published
2024

18. Rapidly progressive multiple system atrophy in a patient carrying LRRK2 G2019S mutation

Author

Carrer, T, Bonato, G, Sandre, M, Emmi, A, Campagnolo, M, Musso, G, Carecchio, M, Parchi, P, Antonini, A, Carrer T., Bonato G., Sandre M., Emmi A., Campagnolo M., Musso G., Carecchio M., Parchi P., Antonini A., Carrer, T, Bonato, G, Sandre, M, Emmi, A, Campagnolo, M, Musso, G, Carecchio, M, Parchi, P, Antonini, A, Carrer T., Bonato G., Sandre M., Emmi A., Campagnolo M., Musso G., Carecchio M., Parchi P., and Antonini A.

Abstract

Background: Multiple system atrophy (MSA) is considered a primarily sporadic neurodegenerative disease, but the role of genetic is poorly understood. Case: We present a female patient of Moroccan origin who developed a rapidly progressive non-levodopa responsive parkinsonism, gait and balance problems, and dysautonomia including severe bulbar symptoms. She was diagnosed with MSA Parkinsonian-type (MSA-P) and suddenly died at night at 58 years of age. Reduced striatal DAT-SPECT, putaminal hyperintensity on T2-MRI, and hypometabolism with FDG-PET were present. Genetic testing documented a G2019S mutation in the LRRK2 gene. A skin biopsy was obtained and used to perform alpha-synuclein RT-QuIC, which was negative, and immunohistochemical analysis, which demonstrated abnormal alpha-synuclein deposits in cutaneous nerves. Elevated blood neurofilament light chain levels were also documented. Conclusions: LRRK2 mutations are the most common cause of monogenic Parkinson’s disease (PD) and G2019S is the most frequent variant. Our patient presented with biological, clinical, and radiological features of MSA, but genetic testing revealed a G2019S LRRK2 mutation, which has been previously reported only in one other case of pathologically proven MSA but with mild progression. In our patient, post-mortem confirmation could not be performed, but RT-QuIC and immunohistochemical findings on skin biopsy support the diagnosis of MSA. G2019S LRRK2 may be linked to an increased risk of MSA. Cases of atypical parkinsonism with rapid disease course should be screened for PD-related genes especially in populations with a high prevalence of mutations in known genes.

Published
2024

20. Sporadic Creutzfeldt-Jakob disease VM1: phenotypic and molecular characterization of a novel subtype of human prion disease

Author

Gelpi, Ellen, Baiardi, Simone, Nos, Carlos, Dellavalle, Sofia, Aldecoa, Iban, Ruiz-Garcia, Raquel, Ispierto, Lourdes, Escudero, Domingo, Casado, Virgina, Barranco, Elena, Boltes, Anuncia, Molina-Porcel, Laura, Bargalló, Nuria, Rossi, Marcello, Mammana, Angela, Tiple, Dorina, Vaianella, Luana, Stoegmann, Elisabeth, Simonitsch-Klupp, Ingrid, Kasprian, Gregor, Klotz, Sigrid, Höftberger, Romana, Budka, Herbert, Kovacs, Gabor G., Ferrer, Isidre, Capellari, Sabina, Sanchez-Valle, Raquel, and Parchi, Piero

Published
2022
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22. In vivo assessment of Lewy body and beta-amyloid copathologies in idiopathic normal pressure hydrocephalus: prevalence and associations with clinical features and surgery outcome

Author

Giannini, Giulia, Baiardi, Simone, Dellavalle, Sofia, Zenesini, Corrado, Cevoli, Sabina, Danner, Nils, Jyrkkänen, Henna-Kaisa, Rossi, Marcello, Polischi, Barbara, Quadalti, Corinne, Stefanini, Camilla, Cortelli, Pietro, Milletti, David, Herukka, Sanna-Kaisa, Palandri, Giorgio, Leinonen, Ville, and Parchi, Piero

Published
2022
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26. Associations between misfolded alpha‐synuclein aggregates and Alzheimer's disease pathology in vivo.

Author

Pichet Binette, Alexa, Mammana, Angela, Wisse, Laura, Rossi, Marcello, Strandberg, Olof, Smith, Ruben, Mattsson‐Carlgren, Niklas, Janelidze, Shorena, Palmqvist, Sebastian, Ticca, Alice, Stomrud, Erik, Parchi, Piero, and Hansson, Oskar

Abstract

INTRODUCTION: We examined the relations of misfolded alpha synuclein (α‐synuclein) with Alzheimer's disease (AD) biomarkers in two large independent cohorts. METHODS: We included Biomarkers for Identifying Neurodegenerative Disorders Early and Reliably Two (BioFINDER‐2) and Alzheimer's Disease Neuroimaging Initiative (ADNI) participants (n = 2315, cognitively unimpaired, mild cognitive impairment, AD dementia) who had cross‐sectional cerebrospinal fluid (CSF) α‐synuclein measurement from seed‐amplification assay as well as cross‐sectional and longitudinal amyloid beta (Aβ) and tau levels (measured in CSF and/or by positron emission tomography). All analyses were adjusted for age, sex, and cognitive status. RESULTS: Across cohorts, the main biomarker associated with α‐synuclein positivity at baseline was higher levels of Aβ pathology (all p values ≤ 0.02), but not tau. Looking at longitudinal measures of AD biomarkers, α‐synuclein –positive participants had a statistically significant faster increase of Aβ load, although of modest magnitude (1.11 Centiloid/year, p = 0.02), compared to α‐synuclein –negative participants in BioFINDER‐2 but not in ADNI. DISCUSSION: We showed associations between concurrent misfolded α‐synuclein and Aβ levels, providing in vivo evidence of links between these two molecular disease pathways in humans. Highlights: Amyloid beta (Aβ), but not tau, was associated with alpha‐synuclein (α‐synuclein) positivity.Such association was consistent across two cohorts, beyond the effect of age, sex, and cognitive status.α‐synuclein–positive participants had a small, statistically significant faster increase in Aβ positron emission tomography levels in one of the two cohorts. [ABSTRACT FROM AUTHOR]

Published
2024
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27. Genome wide association study of clinical duration and age at onset of sporadic CJD

Author

Zanusso, G, Hummerich, H, Speedy, H, Campbell, T, Darwent, L, Hill, E, Collins, S, Stehmann, C, Kovacs, GG, Geschwind, MD, Frontzek, K, Budka, H, Gelpi, E, Aguzzi, A, van der Lee, SJ, van Duijn, CM, Liberski, PP, Calero, M, Sanchez-Juan, P, Bouaziz-Amar, E, Laplanche, J-L, Haik, S, Brandel, J-P, Mammana, A, Capellari, S, Poleggi, A, Ladogana, A, Pocchiari, M, Zafar, S, Booth, S, Jansen, GH, Areskeviciute, A, Lobner Lund, E, Glisic, K, Parchi, P, Hermann, P, Zerr, I, Appleby, BS, Safar, J, Gambetti, P, Collinge, J, Mead, S, Zanusso, G, Hummerich, H, Speedy, H, Campbell, T, Darwent, L, Hill, E, Collins, S, Stehmann, C, Kovacs, GG, Geschwind, MD, Frontzek, K, Budka, H, Gelpi, E, Aguzzi, A, van der Lee, SJ, van Duijn, CM, Liberski, PP, Calero, M, Sanchez-Juan, P, Bouaziz-Amar, E, Laplanche, J-L, Haik, S, Brandel, J-P, Mammana, A, Capellari, S, Poleggi, A, Ladogana, A, Pocchiari, M, Zafar, S, Booth, S, Jansen, GH, Areskeviciute, A, Lobner Lund, E, Glisic, K, Parchi, P, Hermann, P, Zerr, I, Appleby, BS, Safar, J, Gambetti, P, Collinge, J, and Mead, S

Abstract

Human prion diseases are rare, transmissible and often rapidly progressive dementias. The most common type, sporadic Creutzfeldt-Jakob disease (sCJD), is highly variable in clinical duration and age at onset. Genetic determinants of late onset or slower progression might suggest new targets for research and therapeutics. We assembled and array genotyped sCJD cases diagnosed in life or at autopsy. Clinical duration (median:4, interquartile range (IQR):2.5-9 (months)) was available in 3,773 and age at onset (median:67, IQR:61-73 (years)) in 3,767 cases. Phenotypes were successfully transformed to approximate normal distributions allowing genome-wide analysis without statistical inflation. 53 SNPs achieved genome-wide significance for the clinical duration phenotype; all of which were located at chromosome 20 (top SNP rs1799990, pvalue = 3.45x10-36, beta = 0.34 for an additive model; rs1799990, pvalue = 9.92x10-67, beta = 0.84 for a heterozygous model). Fine mapping, conditional and expression analysis suggests that the well-known non-synonymous variant at codon 129 is the obvious outstanding genome-wide determinant of clinical duration. Pathway analysis and suggestive loci are described. No genome-wide significant SNP determinants of age at onset were found, but the HS6ST3 gene was significant (pvalue = 1.93 x 10-6) in a gene-based test. We found no evidence of genome-wide genetic correlation between case-control (disease risk factors) and case-only (determinants of phenotypes) studies. Relative to other common genetic variants, PRNP codon 129 is by far the outstanding modifier of CJD survival suggesting only modest or rare variant effects at other genetic loci.

Published
2024

31. MRI Signature of α-Synuclein Pathology in Asymptomatic Stages and a Memory Clinic Population

Author

Wisse, Laura E. M., Spotorno, Nicola, Rossi, Marcello, Grothe, Michel J., Mammana, Angela, Tideman, Pontus, Baiardi, Simone, Strandberg, Olof, Ticca, Alice, van Westen, Danielle, Mattsson-Carlgren, Niklas, Palmqvist, Sebastian, Stomrud, Erik, Parchi, Piero, and Hansson, Oskar

Abstract

IMPORTANCE: The lack of an in vivo measure for α-synuclein (α-syn) pathology until recently has limited thorough characterization of its brain atrophy pattern, especially during early disease stages. OBJECTIVE: To assess the association of state-of-the-art cerebrospinal fluid (CSF) seed amplification assays (SAA) α-syn positivity (SAA α-syn+) with magnetic resonance imaging (MRI) structural measures, across the continuum from clinically unimpaired (CU) to cognitively impaired (CI) individuals, in 3 independent cohorts, and separately in CU and CI individuals, the latter reflecting a memory clinic population. DESIGN, SETTING, AND PARTICIPANTS: Cross-sectional data were used from the Swedish BioFINDER-2 study (inclusion, 2017-2023) as the discovery cohort and the Swedish BioFINDER-1 study (inclusion, 2007-2015) and Alzheimer’s Disease Neuroimaging Initiative (ADNI; inclusion 2005-2022) as replication cohorts. All cohorts are from multicenter studies, but the BioFINDER cohorts used 1 MRI scanner. CU and CI individuals fulfilling inclusion criteria and without missing data points in relevant metrics were included in the study. All analyses were performed from 2023 to 2024. EXPOSURES: Presence of α-syn pathology, estimated by baseline CSF SAA α-syn. MAIN OUTCOMES AND MEASURES: The primary outcomes were cross-sectional structural MRI measures either through voxel-based morphometry (VBM) or regions of interest (ROI) including an automated pipeline for cholinergic basal forebrain nuclei CH4/4p (nucleus basalis of Meynert [NBM]) and CH1/2/3. Secondary outcomes were domain-specific cross-sectional cognitive measures. Analyses were adjusted for CSF biomarkers of Alzheimer pathology. RESULTS: A total of 2961 participants were included in this study: 1388 (mean [SD] age, 71 [10] years; 702 female [51%]) from the BioFINDER-2 study, 752 (mean [SD] age, 72 [6] years; 406 female [54%]) from the BioFINDER-1 study, and 821 (mean [SD] age, 75 [8] years; 449 male [55%]) from ADNI. In the BioFINDER-2 study, VBM analyses in the whole cohort revealed a specific association between SAA α-syn+ and the cholinergic NBM, even when adjusting for Alzheimer copathology. ROI-based analyses in the BioFINDER-2 study focused on regions involved in the cholinergic system and confirmed that SAA α-syn+ was indeed independently associated with smaller NBM (β = −0.271; 95% CI, −0.399 to −0.142; P <.001) and CH1/2/3 volumes (β = −0.227; 95% CI, −0.377 to −0.076; P =.02). SAA α-syn+ was also independently associated with smaller NBM volumes in the separate CU (β = −0.360; 95% CI, −0.603 to −0.117; P =.03) and CI (β = −0.251; 95% CI, −0.408 to −0.095; P =.02) groups. Overall, the association between SAA α-syn+ and NBM volume was replicated in the BioFINDER-1 study and ADNI cohort. In CI individuals, NBM volumes partially mediated the association of SAA α-syn+ with attention/executive impairments in all cohorts (BioFINDER-2, β = −0.017; proportion-mediated effect, 7%; P =.04; BioFINDER-1, β = −0.096; proportion-mediated effect, 19%; P =.04; ADNI, β = −0.061; proportion-mediated effect, 20%; P =.007). CONCLUSIONS AND RELEVANCE: In this cohort study, SAA α-syn+ was consistently associated with NBM atrophy already during asymptomatic stages. Further, in memory clinic CI populations, SAA α-syn+ was associated with NBM atrophy, which partially mediated α-syn–induced attention/executive impairment.

Published
2024
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32. Duodenal alpha-Synuclein Pathology and Enteric Gliosis in Advanced Parkinson's Disease

Author

Emmi, A, Sandre, M, Russo, F, Tombesi, G, Garri, F, Campagnolo, M, Carecchio, M, Biundo, R, Spolverato, G, Macchi, V, Savarino, E, Farinati, F, Parchi, P, Porzionato, A, Bubacco, L, De Caro, R, Kovacs, G, Antonini, A, Emmi A., Sandre M., Russo F. P., Tombesi G., Garri F., Campagnolo M., Carecchio M., Biundo R., Spolverato G., Macchi V., Savarino E., Farinati F., Parchi P., Porzionato A., Bubacco L., De Caro R., Kovacs G. G., Antonini A., Emmi, A, Sandre, M, Russo, F, Tombesi, G, Garri, F, Campagnolo, M, Carecchio, M, Biundo, R, Spolverato, G, Macchi, V, Savarino, E, Farinati, F, Parchi, P, Porzionato, A, Bubacco, L, De Caro, R, Kovacs, G, Antonini, A, Emmi A., Sandre M., Russo F. P., Tombesi G., Garri F., Campagnolo M., Carecchio M., Biundo R., Spolverato G., Macchi V., Savarino E., Farinati F., Parchi P., Porzionato A., Bubacco L., De Caro R., Kovacs G. G., and Antonini A.

Published
2023

35. Association between CSF alpha-synuclein seeding activity and genetic status in Parkinson’s disease and dementia with Lewy bodies

Author

Brockmann, Kathrin, Quadalti, Corinne, Lerche, Stefanie, Rossi, Marcello, Wurster, Isabel, Baiardi, Simone, Roeben, Benjamin, Mammana, Angela, Zimmermann, Milan, Hauser, Ann-Kathrin, Deuschle, Christian, Schulte, Claudia, Waniek, Katharina, Lachmann, Ingolf, Sjödin, Simon, Brinkmalm, Ann, Blennow, Kaj, Zetterberg, Henrik, Gasser, Thomas, and Parchi, Piero

Published
2021
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36. In vivo detection of Alzheimer's and Lewy body disease concurrence: Clinical implications and future perspectives.

Author

Baiardi, Simone, Hansson, Oskar, Levin, Johannes, and Parchi, Piero

Abstract

INTRODUCTION: The recent introduction of seed amplification assays (SAAs) detecting misfolded α‐synuclein, a pathology‐specific marker for Lewy body disease (LBD), has allowed the in vivo identification and phenotypic characterization of patients with co‐occurring Alzheimer's disease (AD) and LBD since the early clinical or even preclinical stage. METHODS: We reviewed studies with an in vivo biomarker‐based diagnosis of AD‐LBD copathology. RESULTS: Studies in large cohorts of cognitively impaired individuals have shown that cerebrospinal fluid (CSF) biomarkers detect the coexistence of AD and LB pathology in approximately 20%–25% of them, independently of the primary clinical diagnosis. Compared to those with pure AD, AD‐LBD patients showed worse global cognition, especially in attentive/executive and visuospatial functions, and worse motor functions. In cognitively unimpaired individuals, concurrent AD‐LBD pathologies predicted longitudinal cognitive progression with faster worsening of global cognition, memory, and attentive/executive functions. DISCUSSION: Future research studies aiming for a better precision medicine approach should develop SAAs further to reach a quantitative evaluation or staging of each underlying pathology using a single biofluid sample. Highlights: α‐Synuclein seed amplification assays (SAAs) provide a specific marker for Lewy body disease (LBD).SAAs allow for the in vivo identification of co‐occurring LBD in patients with Alzheimer's disease (AD).AD‐LBD coexist in 20‐25% of cognitively impaired elderly individuals, and ∼8% of those asymptomatic.Compared to pure AD, AD‐LBD causes a faster worsening of cognitive functions.AD‐LBD is associated with worse attentive/executive, memory, visuospatial and motor functions. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Levels of plasma brain‐derived tau and p‐tau181 in Alzheimer's disease and rapidly progressive dementias.

Author

Gonzalez‐Ortiz, Fernando, Karikari, Thomas K., Bentivenga, Giuseppe Mario, Baiardi, Simone, Mammana, Angela, Turton, Michael, Kac, Przemysław R., Mastrangelo, Andrea, Harrison, Peter, Capellari, Sabina, Zetterberg, Henrik, Blennow, Kaj, and Parchi, Piero

Abstract

INTRODUCTION: Rapidly progressive dementias (RPDs) are a group of neurological disorders characterized by a rapid cognitive decline. The diagnostic value of blood‐based biomarkers for Alzheimer's disease (AD) in RPD has not been fully explored. METHODS: We measured plasma brain‐derived tau (BD‐tau) and p‐tau181 in 11 controls, 15 AD patients, and 33 with RPD, of which 19 were Creutzfeldt‐Jakob disease (CJD). RESULTS: Plasma BD‐tau differentiated AD from RPD and controls (p = 0.002 and p = 0.03, respectively), while plasma and cerebrospinal fluid (CSF) p‐tau181 distinguished AD from RPD (p < 0.001) but not controls from RPD (p > 0.05). The correlation of CSF t‐tau with plasma BD‐tau was stronger (r = 0.78, p < 0.001) than the correlation of CSF and plasma p‐tau181 (r = 0.26, p = 0.04). The ratio BD‐tau/p‐tau181 performed equivalently to the CSF t‐tau/p‐tau181 ratio, differentiating AD from CJD (p < 0.0001). DISCUSSION: Plasma BD‐tau and p‐tau181 mimic their corresponding cerebrospinal fluid (CSF) markers. P‐tau significantly increased in AD but not in RPD. Plasma BD‐tau, like CSF t‐tau, increases according to neurodegeneration intensity. [ABSTRACT FROM AUTHOR]

Published
2024
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45. Prion-specific and surrogate CSF biomarkers in Creutzfeldt-Jakob disease: diagnostic accuracy in relation to molecular subtypes and analysis of neuropathological correlates of p-tau and Aβ42 levels

Author

Lattanzio, Francesca, Abu-Rumeileh, Samir, Franceschini, Alessia, Kai, Hideaki, Amore, Giulia, Poggiolini, Ilaria, Rossi, Marcello, Baiardi, Simone, McGuire, Lynne, Ladogana, Anna, Pocchiari, Maurizio, Green, Alison, Capellari, Sabina, and Parchi, Piero

Published
2017
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50. Neuropathological assessments of the pathology in frontotemporal lobar degeneration with TDP43-positive inclusions: an inter-laboratory study by the BrainNet Europe consortium

Author

Alafuzoff, Irina, Pikkarainen, Maria, Neumann, Manuela, Arzberger, Thomas, Al-Sarraj, Safa, Bodi, Istvan, Bogdanovic, Nenad, Bugiani, Orso, Ferrer, Isidro, Gelpi, Ellen, Gentleman, Stephen, Giaccone, Giorgio, Graeber, Manuel B., Hortobagyi, Tibor, Ince, Paul G., Ironside, James W., Kavantzas, Nikolaos, King, Andrew, Korkolopoulou, Penelope, Kovács, Gábor G., Meyronet, David, Monoranu, Camelia, Nilsson, Tatjana, Parchi, Piero, Patsouris, Efstratios, Revesz, Tamas, Roggendorf, Wolfgang, Rozemuller, Annemieke, Seilhean, Danielle, Streichenberger, Nathalie, Thal, Dietmar R., Wharton, Stephen B., and Kretzschmar, Hans

Published
2015
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