RICARDO NITRINI
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Neurologia, Faculdade de Medicina - Docente
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/15 - Laboratório de Investigação em Neurologia, Hospital das Clínicas, Faculdade de Medicina
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
Instituto Central, Hospital das Clínicas, Faculdade de Medicina
LIM/15 - Laboratório de Investigação em Neurologia, Hospital das Clínicas, Faculdade de Medicina
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
14 resultados
Resultados de Busca
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- Reader response: Circulating cortisol and cognitive and structural brain measures: The Framingham Heart Study(2019) BARBOSA, Breno J. A. P.; SOUZA-TALARICO, Juliana N. de; NITRINI, Ricardo; BRUCKI, Sonia M. D.
conferenceObject Amyloid-beta Deposition, Brain Metabolism and Neuropsychological Profile in Elderly with Subjective Cognitive Decline and SuperAgers(2020) STUDART-NETO, Adalberto; COUTINHO, Artur; CARNEIRO, Camila de Godoi; MORAES, Natalia Cristina; SPERA, Raphael Ribeiro; YASSUDA, Monica Sanches; BRUCKI, Sonia Maria Dozzi; LEITE, Claudia; BUCHPIGUEL, Carlos; NITRINI, Ricardo- Neuropathologic Findings in a Patient With Juvenile-Onset Levodopa-Responsive Parkinsonism Due to ATP13A2 Mutation(2021) CHIEN, Hsin Fen; RODRIGUEZ, Roberta Diehl; BONIFATI, Vincenzo; NITRINI, Ricardo; PASQUALUCCI, Carlos Augusto; GELPI, Ellen; BARBOSA, Egberto ReisObjective To describe the postmortem neuropathologic findings of a patient with Kufor Rakeb syndrome (KRS) due to ATP13A2 mutation. KRS is characterized by juvenile-onset levodopa-responsive parkinsonism associated with pyramidal signs, supranuclear gaze palsy, and cognitive impairment. Methods A detailed neuropathologic analysis of the brain was performed. The patient had a genetically confirmed ATP13A2 homozygous missense mutation and died at age 38 years, which was 26 years after the onset of his symptoms. Results The main brain neuropathologic findings were widespread neuronal and glial lipofuscin accumulation with no Lewy body-type inclusions and absence of alpha-synuclein-positive, tau-positive, beta-amyloid-positive, and TDP-43 protein-positive pathologies. Sparse iron deposits were observed in several brain areas, but no obvious axonal spheroids were identified. Discussion This is to our knowledge the first KRS postmortem neuropathologic description. Iron deposits were found but not associated with increased axonal spheroids, as frequently observed in neurodegeneration with brain iron accumulation. ATP13A2 mutations have been described in patients with neuronal ceroid lipofuscinosis (CLN). Moreover, animal models with these mutations develop neurodegenerative disorders with CLN pathology. Therefore, our findings support that ATP13A2 mutations may be considered a genetic etiology of neuronal lipofuscinosis.
- Reader response: Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium(2018) PARMERA, Jacy B.; BRUCKI, Sonia; NITRINI, Ricardo
- Very low levels of education and cognitive reserve A clinicopathologic study(2013) FARFEL, Jose Marcelo; NITRINI, Ricardo; SUEMOTO, Claudia Kimie; GRINBERG, Lea Tenenholz; FERRETTI, Renata Eloah Lucena; LEITE, Renata Elaine Paraizo; TAMPELLINI, Edilaine; LIMA, Luzia; FARIAS, Daniela Souza; NEVES, Ricardo Caires; RODRIGUEZ, Roberta Diehl; MENEZES, Paulo Rossi; FREGNI, Felipe; BENNETT, David A.; PASQUALUCCI, Carlos Augusto; JACOB FILHO, WilsonObjective: We conducted a clinicopathologic study in a large population with very low levels of education to determine whether very few years of education could contribute to cognitive reserve and modify the relation of neuropathologic indices to dementia. Methods: In this cross-sectional study, we included 675 individuals 50 years of age or older from the Brazilian Aging Brain Study Group. Cognitive abilities were evaluated through a structured interview with an informant at the time of autopsy, including the Clinical Dementia Rating (CDR) scale. Neuropathologic examinations were performed using immunohistochemistry and following internationally accepted criteria. Multivariate linear regression models were conducted to determine whether the association between cognitive abilities (measured by CDR sum of boxes) and years of education was independent of sociodemographic variables and neuropathologic indices, including neuritic plaques, neurofibrillary tangles, lacunar infarctions, small-vessel disease, and Lewy bodies. In addition, interaction models were used to examine whether education modified the relation between neuropathologic indices and cognition. Results: Mean education was 3.9 +/- 3.5 years. Formal education was associated with a lower CDR sum of boxes (beta = -0.197; 95% confidence interval -0.343, -0.052; p = 0.008), after adjustment for sociodemographic variables and neuropathologic indices. Furthermore, education modified the relationship of lacunar infarcts with cognitive abilities (p = 0.04). Conclusions: Even a few years of formal education contributes to cognitive reserve.
- Teaching Video NeuroImages: Susac syndrome's acute onset callosal disconnection(2020) MOURAO, Lucas Oliveira; PARMERA, Jacy Bezerra; BERGAMASCHI, Eduardo de Novaes Costa; NUNES, Douglas Mendes; NITRINI, Ricardo; BRUCKI, Sonia M. D.A 59-year-old right-handed hypertensive diabetic and previously alcoholic man presented acute confusional state followed by apathy, dysexecutive syndrome, clumsy left hand, and apraxic gait. A year later, his wife noticed impaired hearing. Neurologic examination revealed marked callosal apraxia (nondominant limb ideomotor apraxia, disconnection variant) and left stereoagnosis due to callosal disconnection (video). Left hand agraphia was present without aphasia. MRI showed punched out holes through corpus callosum, sparing the calloso-septal interface (figure 1). Audiometry revealed left neurosensorial loss. Fluorescein retinography demonstrated hyperfluorescence of arterial vessel wall (figure 2), confirming the hypothesis of Susac syndrome.(1)
- Dementia in Latin America: Assessing the present and envisioning the future(2018) PARRA, Mario A.; BAEZ, Sandra; ALLEGRI, Ricardo; NITRINI, Ricardo; LOPERA, Francisco; SLACHEVSKY, Andrea; CUSTODIO, Nilton; LIRA, David; PIGUET, Olivier; KUMFOR, Fiona; HUEPE, David; COGRAM, Patricia; BAK, Thomas; MANES, Facundo; IBANEZ, AgustinThe demographic structure of Latin American countries (LAC) is fast approaching that of developing countries, and the predicted prevalence of dementia in the former already exceeds the latter. Dementia has been declared a global challenge, yet regions around the world show differences in both the nature and magnitude of such a challenge. This article provides evidence and insights on barriers which, if overcome, would enable the harmonization of strategies to tackle the dementia challenge in LAC. First, we analyze the lack of available epidemiologic data, the need for standardizing clinical practice and improving physician training, and the existing barriers regarding resources, culture, and stigmas. We discuss how these are preventing timely care and research. Regarding specific health actions, most LAC have minimal mental health facilities and do not have specific mental health policies or budgets specific to dementia. In addition, local regulations may need to consider the regional context when developing treatment and prevention strategies. The support needed nationally and internationally to enable a smooth and timely transition of LAC to a position that integrates global strategies is highlighted. We focus on shared issues of poverty, cultural barriers, and socioeconomic vulnerability. We identify avenues for collaboration aimed to study unique populations, improve valid assessment methods, and generate opportunities for translational research, thus establishing a regional network. The issues identified here point to future specific actions aimed at tackling the dementia challenge in LAC.
conferenceObject Assessment of Diagnostic Value and Risks of Brain Biopsy in Neurologic Disease(2016) GUEDES, Bruno; SILVA, Andre; SOLLA, Davi; CASTRO, Luiz; SOARES-NETO, Herval; NETO, Adalberto Studart; TINONE, Gisela; GONCALVES, Marcia; FORTINI, Ida; NITRINI, Ricardo- Teaching NeuroImages: Bilateral intracerebral hemorrhage in expanded dengue syndrome(2017) CAVALCANTE, Wagner Cid Palmeira; SOARES NETO, Herval Ribeiro; GRATIVVOL, Ronnyson Susano; SPERA, Raphael Ribeiro; FRASSETTO, Fernando Pereira; LUCATO, Leandro Tavares; NITRINI, Ricardo
- Spontaneous ARIA-like Events in Cerebral Amyloid Angiopathy-Related Inflammation A Multicenter Prospective Longitudinal Cohort Study(2021) ANTOLINI, Laura; DIFRANCESCO, Jacopo C.; ZEDDE, Marialuisa; BASSO, Gianpaolo; ARIGHI, Andrea; SHIMA, Atsushi; CAGNIN, Annachiara; CAULO, Massimo; CARARE, Roxana O.; CHARIDIMOU, Andreas; CIRILLO, Mario; LAZZARO, Vincenzo Di; FERRARESE, Carlo; GIOSSI, Alessia; INZITARI, Domenico; MARCON, Michela; MARCONI, Roberto; IHARA, Masafumi; NITRINI, Ricardo; ORLANDI, Berardino; PADOVANI, Alessandro; PASCARELLA, Rosario; PERINI, Francesco; PERINI, Giulia; SESSA, Maria; SCARPINI, Elio; TAGLIAVINI, Fabrizio; VALENTI, Raffaella; VAZQUEZ-COSTA, Juan Francisco; VILLAREJO-GALENDE, Alberto; HAGIWARA, Yuta; ZILIOTTO, Nicole; PIAZZA, FabrizioBackground and Objectives The goal of this work was to investigate the natural history and outcomes after treatment for spontaneous amyloid-related imaging abnormalities (ARIA)-like in cerebral amyloid angiopathy-related inflammation (CAA-ri). Methods This was a multicenter, hospital-based, longitudinal, prospective observational study of inpatients meeting CAA-ri diagnostic criteria recruited through the Inflammatory Cerebral Amyloid Angiopathy and Alzheimer's Disease beta iomarkers International Network from January 2013 to March 2017. A protocol for systematic data collection at first-ever presentation and at subsequent in-person visits, including T1-weighted, gradient recalled echo-T2*, fluid-suppressed T2-weighted (fluid-attenuated inversion recovery), and T1 postgadolinium contrast-enhanced images acquired on 1.5T MRI, was used at the 3-, 6-, 12-, and 24-month follow-up. Centralized reads of MRIs were performed by investigators blinded to clinical, therapeutic, and time-point information. Main outcomes were survival, clinical and radiologic recovery, intracerebral hemorrhage (ICH), and recurrence of CAA-ri. Results The study enrolled 113 participants (10.6% definite, 71.7% probable, and 17.7% possible CAA-ri). Their mean age was 72.9 years; 43.4% were female; 37.1% were APOE epsilon 4 carriers; 36.3% had a history of Alzheimer disease; and 33.6% had a history of ICH. A history of ICH and the occurrence of new ICH at follow-up were more common in patients with cortical superficial siderosis at baseline (52.6% vs 14.3%, p < 0.0001 and 19.3% vs 3.6%, p < 0.009, respectively). After the first-ever presentation of CAA-ri, 70.3% (95% confidence interval [CI] 61.6%-78.5%) and 84.1% (95% CI 76.2%-90.6%) clinically recovered within 3 and 12 months, followed by radiologic recovery in 45.1% (95% CI 36.4%-54.8%) and 77.4% (95% CI 67.7%-85.9%), respectively. After clinicoradiologic resolution of the first-ever episode, 38.3% (95% CI 22.9%-59.2%) had at least 1 recurrence within the following 24 months. Recurrence was more likely if IV high-dose corticosteroid pulse therapy was suddenly stopped compared to slow oral tapering off (hazard ratio 4.68, 95% CI 1.57-13.93; p = 0.006). Discussion These results from the largest longitudinal cohort registry of patients with CAA-ri support the transient and potentially relapsing inflammatory nature of the clinical-radiologic acute manifestations of the disease and the effectiveness of slow oral tapering off after IV corticosteroid pulse therapy in preventing recurrences. Our results highlight the importance of differential diagnosis for spontaneous ARIA-like events in beta-amyloid-driven diseases, including treatment-related ARIA in patients with Alzheimer disease exposed to immunotherapy drugs.