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5. Reactive microglia partially envelop viable neurons in prion diseases

Author

Makarava, Natallia, Safadi, Tarek, Bocharova, Olga, Mychko, Olga, Pandit, Narayan P., Molesworth, Kara, Baiardi, Simone, Zhang, Li, Parchi, Piero, and Baskakov, Ilia V.

Subjects
Brain, Medical research, Medicine, Experimental, Neurons, Nervous system diseases -- Development and progression, Health care industry
Abstract

Microglia are recognized as the main cells in the central nervous system responsible for phagocytosis. The current study demonstrates that in prion disease, microglia effectively phagocytose prions or [PrP.sup.Sc] during early preclinical stages. However, a critical shift occurred in microglial activity during the late preclinical stage, transitioning from [PrP.sup.Sc] uptake to establishing extensive neuron-microglia body-to-body cell contacts. This change was followed by a rapid accumulation of [PrP.sup.Sc] in the brain. Microglia that enveloped neurons exhibited hypertrophic, cathepsin D-positive lysosomal compartments. However, most neurons undergoing envelopment were only partially encircled by microglia. Despite up to 40% of cortical neurons being partially enveloped at clinical stages, only a small percentage of envelopment proceeded to full engulfment. Partially enveloped neurons lacked apoptotic markers, but showed signs of functional decline. Neuronal envelopment was independent of the CD11b pathway, previously associated with phagocytosis of newborn neurons during neurodevelopment. This phenomenon of partial envelopment was consistently observed across multiple prion-affected brain regions, various mouse-adapted strains, and different subtypes of sporadic Creutzfeldt-Jakob disease (sCJD) in humans. The current work describes a phenomenon of partial envelopment of neurons by reactive microglia in the context of an actual neurodegenerative disease, not a disease model., Introduction Microglia are recognized as the main cells in the CNS responsible for phagocytosis. In early brain development, microglia are crucial in optimizing neural circuitry and eliminating excessive synapses, neurons, [...]

Published
2024
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8. Sensitivity and specificity of a seed amplification assay for diagnosis of multiple system atrophy: a multicentre cohort study

Author

Ma, Yihua, Farris, Carly M, Weber, Sandrina, Schade, Sebastian, Nguyen, Hieu, Pérez-Soriano, Alexandra, Giraldo, Darly M, Fernández, Manel, Soto, Marta, Cámara, Ana, Painous, Celia, Muñoz, Esteban, Valldeoriola, Francesc, Martí, Maria J, Clarimon, Jordi, Kallunki, Pekka, Ma, Thong Chi, Alcalay, Roy N, Gomes, Bárbara Fernandez, Blennow, Kaj, Zetterberg, Henrik, Constantinescu, Julius, Mengel, David, Kadam, Vaibhavi, Parchi, Piero, Brockmann, Kathrin, Tropea, Thomas F, Siderowf, Andrew, Synofzik, Matthis, Kang, Un Jung, Compta, Yaroslau, Svenningsson, Per, Mollenhauer, Brit, and Concha-Marambio, Luis

Published
2024
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16. 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

17. 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

18. Role of Blood P-Tau Isoforms (181, 217, 231) in Predicting Conversion from MCI to Dementia Due to Alzheimer's Disease: A Review and Meta-Analysis.

Author

Lombardi, Gemma, Pancani, Silvia, Manca, Riccardo, Mitolo, Micaela, Baiardi, Simone, Massa, Federico, Coppola, Luigi, Franzese, Monica, Nicolai, Emanuele, Guerini, Franca Rosa, Mancuso, Roberta, Agliardi, Cristina, Agostini, Simone, Pardini, Matteo, Virgili, Gianni, Sorbi, Sandro, Parchi, Piero, Nacmias, Benedetta, and Venneri, Annalena

Abstract

Blood-based biomarkers are minimally invasive tools to detect the pathological changes of Alzheimer's Disease (AD). This meta-analysis aims to investigate the use of blood-derived p-tau isoforms (181, 217, 231) to predict conversion from mild cognitive impairment (MCI) to AD dementia (ADD). Studies involving MCI patients with data on blood p-tau isoforms at baseline and clinical diagnosis at follow-up (≥1 year) were included. Twelve studies on p-tau 181 (4340 MCI, conversion rate 20.6%), four on p-tau 217 (913 MCI, conversion rate 33.4%), and one on p-tau 231 (135 MCI, conversion rate 33%) were included. For p-tau 181, the pooled area under the receiver operating characteristic curve (AUC) was 0.73 (95% CI = 0.68–0.78), and for p-tau 217 was 0.85 (95% CI = 0.75–0.91). Plasma levels of p-tau 181 had good discriminatory power to identify MCI patients who will convert to ADD. Although only four studies on p-tau 217 have been included in the meta-analysis, in the last year the predictive power of p-tau 217 is emerging as superior to that of other isoforms. However, given the high heterogeneity detected in the p-tau 217 studies included in this meta-analysis, additional supportive evidence is needed. Insufficient results were available for p-tau 231. These findings support the prognostic utility of p-tau 181 and p-tau 217 measured in blood to predict progression to ADD in MCI and encourage its future implementation in clinical practice. [ABSTRACT FROM AUTHOR]

Published
2024
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19. 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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21. 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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29. Improving protocols for α-synuclein seed amplification assays: analysis of preanalytical and analytical variables and identification of candidate parameters for seed quantification.

Author

Mammana, Angela, Baiardi, Simone, Rossi, Marcello, Quadalti, Corinne, Ticca, Alice, Magliocchetti, Franco, Bernhardt, Alexander, Capellari, Sabina, and Parchi, Piero

Subjects
PARKINSON'S disease, FREEZE-thaw cycles, RECOMBINANT proteins, CEREBROSPINAL fluid, PARAMETER identification
Abstract

The effect of preanalytical and analytical factors on the α-synuclein (α-syn) seed amplification assay's (SAA) performance has not been fully explored. Similarly, there is limited knowledge about the most suitable assay protocol and kinetic parameters for misfolded α-syn seed quantification. We studied the effect of centrifugation, repeated freeze-thaw cycles (up to seven), delayed freezing, detergent addition, and blood contamination on the performance of the cerebrospinal fluid (CSF) α-syn SAA real-time quaking-induced conversion (RT-QuIC). Moreover, we analysed the inter- and intra-plate variability, the recombinant protein batch effect, and the RT-QuIC parameters' variability when multiple samples were run in controlled conditions. Finally, we evaluated the assay potential of quantifying α-syn seed by assessing kinetic curves in serial CSF dilutions. Among tested preanalytical variables, a ≥0.01 % blood contamination and adding detergents significantly affected the RT-QuIC kinetic parameters and the number of positive replicates. Increasing the number of replicates improved result reproducibility. The number of positive replicates in serially diluted CSF samples improved discrimination between samples with high and low seeding activity, and the time to threshold (LAG) was the most reliable kinetic parameter in multiple experiment settings. Preanalytical variables affecting α-syn RT-QuIC performance are limited to blood contamination and detergent addition. The number of positive replicates and the LAG are the most reliable variables for quantifying α-syn seeding activity. Their consistent measurement in serial dilution experiments, especially when associated with an increased number of sample replicates, will help to develop the α-syn RT-QuIC assay further into a quantitative test. [ABSTRACT FROM AUTHOR]

Published
2024
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30. 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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31. Identification of novel risk loci and causal insights for sporadic Creutzfeldt-Jakob disease: a genome-wide association study

Author

Jones, Emma, Hummerich, Holger, Viré, Emmanuelle, Uphill, James, Dimitriadis, Athanasios, Speedy, Helen, Campbell, Tracy, Norsworthy, Penny, Quinn, Liam, Whitfield, Jerome, Linehan, Jacqueline, Jaunmuktane, Zane, Brandner, Sebastian, Jat, Parmjit, Nihat, Akin, How Mok, Tze, Ahmed, Parvin, Collins, Steven, Stehmann, Christiane, Sarros, Shannon, Kovacs, Gabor G, Geschwind, Michael D, Golubjatnikov, Aili, Frontzek, Karl, Budka, Herbert, Aguzzi, Adriano, Karamujić-Čomić, Hata, van der Lee, Sven J, Ibrahim-Verbaas, Carla A, van Duijn, Cornelia M, Sikorska, Beata, Golanska, Ewa, Liberski, Pawel P, Calero, Miguel, Calero, Olga, Sanchez-Juan, Pascual, Salas, Antonio, Martinón-Torres, Federico, Bouaziz-Amar, Elodie, Haïk, Stéphane, Laplanche, Jean-Louis, Brandel, Jean-Phillipe, Amouyel, Phillipe, Lambert, Jean-Charles, Parchi, Piero, Bartoletti-Stella, Anna, Capellari, Sabina, Poleggi, Anna, Ladogana, Anna, Pocchiari, Maurizio, Aneli, Serena, Matullo, Giuseppe, Knight, Richard, Zafar, Saima, Zerr, Inga, Booth, Stephanie, Coulthart, Michael B, Jansen, Gerard H, Glisic, Katie, Blevins, Janis, Gambetti, Pierluigi, Safar, Jiri, Appleby, Brian, Collinge, John, and Mead, Simon

Published
2020
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32. Anterior Callosal Angle: A New Marker of Idiopathic Normal Pressure Hydrocephalus?

Author

Agati, Raffaele, Calandra-Buonaura, Giovanna, Capellari, Sabina, Chiari, Lorenzo, Ferrari, Alberto, Merola, Margherita, Parchi, Piero, Pirina, Alessandro, Piserchia, Vito Antonio, Ricci, Valentina, Sambati, Luisa, Sturiale, Carmelo, Supino, Antonella, Mantovani, Paolo, Albini-Riccioli, Luca, Giannini, Giulia, Milletti, David, Sorenson, Thomas J., Stanzani-Maserati, Michelangelo, Oppi, Federico, Elder, Benjamin D., Cevoli, Sabina, Cortelli, Pietro, and Palandri, Giorgio

Published
2020
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34. Genome wide association study of clinical duration and age at onset of sporadic CJD

Author

Hummerich, Holger, Speedy, Helen, Campbell, Tracy, Darwent, Lee, Hill, Elizabeth, Collins, Steven, Stehmann, Christiane, Kovacs, Gabor G., Geschwind, Michael D., Frontzek, Karl, Budka, Herbert, Gelpi, Ellen, Aguzzi, Adriano, van der Lee, Sven J., van Duijn, Cornelia M., Liberski, Pawel P., Calero, Miguel, Sanchez-Juan, Pascual, Bouaziz-Amar, Elodie, Laplanche, Jean Louis, Haïk, Stéphane, Brandel, Jean Phillipe, Mammana, Angela, Capellari, Sabina, Poleggi, Anna, Ladogana, Anna, Pocchiari, Maurizio, Zafar, Saima, Booth, Stephanie, Jansen, Gerard H., Areškevičiūtė, Aušrinė, Lund, Eva Løbner, Glisic, Katie, Parchi, Piero, Hermann, Peter, Zerr, Inga, Appleby, Brian S., Safar, Jiri, Gambetti, Pierluigi, Collinge, John, Mead, Simon, Hummerich, Holger, Speedy, Helen, Campbell, Tracy, Darwent, Lee, Hill, Elizabeth, Collins, Steven, Stehmann, Christiane, Kovacs, Gabor G., Geschwind, Michael D., Frontzek, Karl, Budka, Herbert, Gelpi, Ellen, Aguzzi, Adriano, van der Lee, Sven J., van Duijn, Cornelia M., Liberski, Pawel P., Calero, Miguel, Sanchez-Juan, Pascual, Bouaziz-Amar, Elodie, Laplanche, Jean Louis, Haïk, Stéphane, Brandel, Jean Phillipe, Mammana, Angela, Capellari, Sabina, Poleggi, Anna, Ladogana, Anna, Pocchiari, Maurizio, Zafar, Saima, Booth, Stephanie, Jansen, Gerard H., Areškevičiūtė, Aušrinė, Lund, Eva Løbner, Glisic, Katie, Parchi, Piero, Hermann, Peter, Zerr, Inga, Appleby, Brian S., Safar, Jiri, Gambetti, Pierluigi, Collinge, John, and Mead, Simon

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

39. 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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41. A prospective evaluation of clinical and instrumental features before and after ventriculo-peritoneal shunt in patients with idiopathic Normal pressure hydrocephalus: The Bologna PRO-Hydro study

Author

Agati, Raffaele, Calandra-Buonaura, Giovanna, Capellari, Sabina, Parchi, Piero, Stanzani-Maserati, Michelangelo, Marliani, Anna Federica, Merola, Margherita, Piserchia, Vito Antonio, Sambati, Luisa, Sturiale, Carmelo, Supino, Antonella, Nicola, Monica, Urli, Tiziana, Giannini, Giulia, Palandri, Giorgio, Ferrari, Alberto, Oppi, Federico, Milletti, David, Albini-Riccioli, Luca, Mantovani, Paolo, Magnoni, Stefania, Chiari, Lorenzo, Cortelli, Pietro, and Cevoli, Sabina

Published
2019
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43. Predicting conversion from mild cognitive impairment to Alzheimer's disease using brain 1H-MRS and volumetric changes: A two- year retrospective follow-up study

Author

Mitolo, Micaela, Stanzani-Maserati, Michelangelo, Capellari, Sabina, Testa, Claudia, Rucci, Paola, Poda, Roberto, Oppi, Federico, Gallassi, Roberto, Sambati, Luisa, Rizzo, Giovanni, Parchi, Piero, Evangelisti, Stefania, Talozzi, Lia, Tonon, Caterina, Lodi, Raffaele, and Liguori, Rocco

Published
2019
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45. High diagnostic performance of plasma and cerebrospinal fluid beta‐synuclein in the differential diagnosis of sporadic Creutzfeldt‐Jakob disease

Author

Rumeileh, Samir Abu, primary, Halbgebauer, Steffen, additional, Bentivenga, Giuseppe, additional, Barba, Lorenzo, additional, Baiardi, Simone, additional, Mastrangelo, Andrea, additional, Oeckl, Patrick, additional, Steinacker, Petra, additional, Mammana, Angela, additional, Capellari, Sabina, additional, Otto, Markus, additional, and Parchi, Piero, additional

Published
2023
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47. LRP10 genetic variants in familial Parkinson's disease and dementia with Lewy bodies: a genome-wide linkage and sequencing study

Author

Bonifati, Vincenzo, Quadri, Marialuisa, Mandemakers, Wim, Kievit, Anneke J.A., Boon, Agnita J.W., Rood, Janneke P.A, Vergouw, Leonie J.M., de Jong, Frank J., van Swieten, John C., Mattace-Raso, Francesco U.S., Leenders, Klaus L., Ferreira, Joaquim J., Correia Guedes, Leonor, Puschmann, Andreas, Ygland, Emil, Nilsson, Christer, Chien, Hsin F., Barbosa, Egberto, Bannach Jardim, Laura, Rieder, Carlos R.M., Chang, Hsiu-Chen, Lu, Chin-Song, Wu-Chou, Yah-Huei, Yeh, Tu-Hsueh, Lopiano, Leonardo, Tassorelli, Cristina, Pacchetti, Claudio, Riboldazzi, Giulio, Bono, Giorgio, Comi, Cristoforo, Padovani, Alessandro, Borroni, Barbara, Raudino, Francesco, Fincati, Emiliana, Tinazzi, Michele, Bonizzato, Alberto, Ferracci, Carlo, Dalla Libera, Alessio, Abbruzzese, Giovanni, Cortelli, Pietro, Capellari, Sabina, Marconi, Roberto, Guidi, Marco, Onofrj, Marco, Thomas, Astrid, Vanacore, Nicola, Meco, Giuseppe, Fabrizio, Edito, Fabbrini, Giovanni, Berardelli, Alfredo, Stocchi, Fabrizio, Vacca, Laura, Barone, Paolo, Picillo, Marina, De Michele, Giuseppe, Criscuolo, Chiara, De Mari, Michele, Dell'Aquila, Claudia, Iliceto, Gianni, Toni, Vincenzo, Trianni, Giorgio, Gagliardi, Monica, Annesi, Grazia, Quattrone, Aldo, Saddi, Valeria, Cossu, Gianni, Melis, Maurizio, Grochowska, Martyna M, Masius, Roy, Geut, Hanneke, Breedveld, Guido J, Kuipers, Demy, Minneboo, Michelle, Vergouw, Leonie J M, Carreras Mascaro, Ana, Yonova-Doing, Ekaterina, Simons, Erik, Zhao, Tianna, Di Fonzo, Alessio B, Parchi, Piero, Melis, Marta, Brouwer, Rutger W W, Heijsman, Daphne, Ingrassia, Angela M T, Calandra Buonaura, Giovanna, Rood, Janneke P, Rozemuller, Annemieke J, Sarchioto, Marianna, Fen Chien, Hsin, Olgiati, Simone, Boon, Agnita J W, Hoogers, Susanne E, Ghazvini, Mehrnaz, IJpma, Arne S, van IJcken, Wilfred F J, Nicholl, David J, Kievit, Anneke J, Majoor-Krakauer, Danielle, van Swieten, John C, de Jong, Frank J, Ferreira, Joaquim J, Cossu, Giovanni, and van de Berg, Wilma D J

Published
2018
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50. Levels of plasma brain‐derived tau and p‐tau181 in Alzheimer's disease and rapidly progressive dementias

Author

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

Published
2023
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