LEONEL TADAO TAKADA
Projetos de Pesquisa
Unidades Organizacionais
Instituto Central, Hospital das Clínicas, Faculdade de Medicina - Médico
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
LIM/45 - Laboratório de Fisiopatologia Neurocirúrgica, Hospital das Clínicas, Faculdade de Medicina
47 resultados
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- Classification of Alzheimer's disease and frontotemporal dementia using routine clinical and cognitive measures across multicentric underrepresented samples: A cross sectional observational study(2023) MAITO, Marcelo Adrian; SANTAMARIA-GARCIA, Hernando; MOGUILNER, Sebastian; POSSIN, Katherine L.; GODOY, Maria E.; AVILA-FUNES, Jose Alberto; I, Maria Behrens; BRUSCO, Ignacio L.; BRUNO, Martin A.; CARDONA, Juan F.; CUSTODIO, Nilton; GARCIA, Adolfo M.; JAVANDEL, Shireen; LOPERA, Francisco; MATALLANA, Diana L.; MILLER, Bruce; OLIVEIRA, Maira Okada de; PINA-ESCUDERO, Stefanie D.; SLACHEVSKY, Andrea; ORTIZ, Ana L. Sosa; TAKADA, Leonel T.; TAGLIAZUCHI, Enzo; VALCOUR, Victor; YOKOYAMA, Jennifer S.; IBANEZ, AgustinBackground Global brain health initiatives call for improving methods for the diagnosis of Alzheimer & rsquo;s disease (AD) and frontotemporal dementia (FTD) in underrepresented populations. However, diagnostic procedures in upper -middle-income countries (UMICs) and lower-middle income countries (LMICs), such as Latin American countries (LAC), face multiple challenges. These include the heterogeneity in diagnostic methods, lack of clinical harmonisation, and limited access to biomarkers. Methods This cross-sectional observational study aimed to identify the best combination of predictors to discriminate between AD and FTD using demographic, clinical and cognitive data among 1794 participants [904 diagnosed with AD, 282 diagnosed with FTD, and 606 healthy controls (HCs)] collected in 11 clinical centres across five LAC (ReDLat cohort). Findings A fully automated computational approach included classical statistical methods, support vector machine procedures, and machine learning techniques (random forest and sequential feature selection procedures). Results demonstrated an accurate classification of patients with AD and FTD and HCs. A machine learning model produced the best values to differentiate AD from FTD patients with an accuracy = 0.91. The top features included social cognition, neuropsychiatric symptoms, executive functioning performance, and cognitive screening; with secondary contributions from age, educational attainment, and sex. Interpretation Results demonstrate that data-driven techniques applied in archival clinical datasets could enhance diagnostic procedures in regions with limited resources. These results also suggest specific fine-grained cognitive and behavioural measures may aid in the diagnosis of AD and FTD in LAC. Moreover, our results highlight an opportunity for harmonisation of clinical tools for dementia diagnosis in the region.
bookPart Doença de Alzheimer(2021) TAKADA, Leonel Tadao; SMID, Jerusa; STUDART NETO, Adalberto; NITRINI, Ricardo- Chronic Traumatic Encephalopathy Presenting as Alzheimer's Disease in a Retired Soccer Player(2016) GRINBERG, Lea T.; ANGHINAH, Renato; NASCIMENTO, Camila Fernandes; AMARO JR., Edson; LEITE, Renata P.; MARTIN, Maria da Graca M.; NASLAVSKY, Michel S.; TAKADA, Leonel T.; JACOB FILHO, Wilson; PASQUALUCCI, Carlos A.; NITRINI, RicardoThe relationship between soccer and chronic traumatic encephalopathy (CTE) is not well established. We report clinicopathological correlations in an 83-year-old retired center-back soccer player, with no history of concussion, manifesting typical Alzheimer-type dementia. Examination revealed mixed pathology including widespread CTE, moderate Alzheimer's disease, hippocampal sclerosis, and TDP-43 proteinopathy. This case adds to a few CTE cases described in soccer players. Furthermore, it corroborates that CTE may present clinically as typical Alzheimer-type dementia. Further studies investigating the extent to which soccer is a risk for CTE are needed.
- Genetic investigation of dementias in clinical practice(2022) TAKADA, Leonel TadaoBackground: The field of neurodegenerative dementia genetics has advanced significantly over the past two decades, but there are still more to be discovered (such as the gene mutation in some familial forms of dementia). Objective: To provide a brief review of the most recent discoveries regarding monogenic dementia, and covering the most frequent genetic diseases that can cause dementia (neurodegenerative or not). Methods: A review of the literature will be carried out.Results: Neurodegenerative dementias, vascular dementias and leukoencephalopathies caused by single pathogenic variants are presented. Conclusion: The spectrum of clinical presentations for most of the genes discussed is wide, and hence genetic testing in clinic should try to cover as many genes as possible.
- Genetic PrP Prion Diseases(2018) KIM, Mee-Ohk; TAKADA, Leonel T.; WONG, Katherine; FORNER, Sven A.; GESCHWIND, Michael D.Genetic prion diseases (gPrDs) caused by mutations in the prion protein gene (PRNF, have been classified as genetic Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker disease, or fatal familial insomnia. Mutations in PRNP can be missense, nonsense, and/or octapeptide repeat insertions or, possibly, deletions. These mutations can produce diverse clinical features. They may also show varying ancillary testing results and neuropathological findings. Although the majority of gPrDs have a rapid progression with a short survival time of a few months, many also present as ataxic or parkinsonian disorders, which have a slower decline over a few to several years. A few very rare mutations manifest as neuropsychiatric disorders, with systemic symptoms that include gastrointestinal disorders and neuropathy; these forms can progress over years to decades. In this review, we classify gPrDs as rapid, slow, or mixed types based on their typical rate of progression and duration, and we review the broad spectrum of phenotypes manifested by these diseases.
- A review on shared clinical and molecular mechanisms between bipolar disorder and frontotemporal dementia(2019) NASCIMENTO, Camila; NUNES, Paula Villela; RODRIGUEZ, Roberta Diehl; TAKADA, Leonel; SUEMOTO, Claudia Kimie; GRINBERG, Lea Tenenholz; NITRINI, Ricardo; LAFER, BenyMental disorders are highly prevalent and important causes of medical burden worldwide. Co-occurrence of neurological and psychiatric symptoms are observed among mental disorders, representing a challenge for their differential diagnosis. Psychiatrists and neurologists have faced challenges in diagnosing old adults presenting behavioral changes. This is the case for early frontotemporal dementia (FTD) and bipolar disorder. In its initial stages, FTD is characterized by behavioral or language disturbances in the absence of cognitive symptoms. Consequently, patients with the behavioral subtype of FTD (bv-FTD) can be initially misdiagnosed as having a psychiatric disorder, typically major depression disorder (MDD) or bipolar disorder (BD). Bipolar disorder is associated with a higher risk of dementia in older adults and with cognitive impairment, with a subset of patients presents a neuroprogressive pattern during the disease course. No mendelian mutations were identified in BD, whereas three major genetic causes of FTD have been identified. Clinical similarities between BD and bv-FTD raise the question whether common molecular pathways might explain shared clinical symptoms. Here, we reviewed existing data on clinical and molecular similarities between BD and FTD to propose biological pathways that can be further investigated as common or specific markers of BD and FTD.
- Atypical, slowly progressive behavioural variant frontotemporal dementia associated with C9ORF72 hexanucleotide expansion(2012) KHAN, Baber K.; YOKOYAMA, Jennifer S.; TAKADA, Leonel T.; SHA, Sharon J.; RUTHERFORD, Nicola J.; FONG, Jamie C.; KARYDAS, Anna M.; WU, Teresa; KETELLE, Robin S.; BAKER, Matthew C.; HERNANDEZ, Mariely-Dejesus; COPPOLA, Giovanni; GESCHWIND, Daniel H.; RADEMAKERS, Rosa; LEE, Suzee E.; ROSEN, Howard J.; RABINOVICI, Gil D.; SEELEY, William W.; RANKIN, Katherine P.; BOXER, Adam L.; MILLER, Bruce L.Background Some patients meeting behavioural variant frontotemporal dementia (bvFTD) diagnostic criteria progress slowly and plateau at mild symptom severity. Such patients have mild neuropsychological and functional impairments, lack characteristic bvFTD brain atrophy and have thus been referred to as bvFTD 'phenocopies' or slowly progressive (bvFTD-SP). The few patients with bvFTD-SP that have been studied at autopsy have demonstrated no evidence of FTD pathology, suggesting that bvFTD-SP is neuropathologically distinct from other forms of FTD. Here, two patients with bvFTD-SP with chromosome 9 open reading frame 72 (C9ORF72) hexanucleotide expansions are described. Methods 384 patients with an FTD clinical spectrum and Alzheimer's disease diagnoses were screened for C9ORF72 expansion. Two bvFTD-SP mutation carriers were identified. Neuropsychological and functional data, as well as brain atrophy patterns, assessed using voxel based morphometry (VBM), were compared with 44 patients with sporadic bvFTD and 85 healthy controls. Results Both patients were aged 48 years at baseline and met possible bvFTD criteria. In the first patient, VBM revealed thalamic and posterior insula atrophy. Over 7 years, his neuropsychological performance and brain atrophy remained stable. In the second patient, VBM revealed cortical atrophy with subtle frontal and insular volume loss. Over 2 years, her neuropsychological and functional scores as well as brain atrophy remained stable. Conclusions C9ORF72 mutations can present with a bvFTD-SP phenotype. Some bvFTD-SP patients may have neurodegenerative pathology, and C9ORF72 mutations should be considered in patients with bvFTD-SP and a family history of dementia or motor neuron disease.
- Frequency of the LRRK2 G2019S mutation in late-onset sporadic patients with Parkinson's disease(2014) CHIEN, Hsin Fen; FIGUEIREDO, Tamires Rocha; HOLLAENDER, Marianna Almeida; TOFOLI, Fabiano; TAKADA, Leonel Tadao; PEREIRA, Lygia do Veiga; BARBOSA, Egberto ReisMutations in the LRRK2 gene, predominantly G2019S, have been reported in individuals with autosomal dominant inheritance and sporadic Parkinson's disease (PD). The G2019S mutation has an age-dependent penetrance and evidence shows common ancestry. The clinical manifestations are indistinguishable from idiopathic PD. Its prevalence varies according to the population studied ranging from less than 0.1% in Asians to 41% in North African Arabs. This study aimed to identify G2019S mutation in Brazilian idiopathic PD patients. Method: We sampled 100 PD patients and 100 age- and gender-matched controls. Genetical analysis was accomplished by polymerase chain reaction (PCR). Results: No G2019S mutations were found in both patients with sporadic PD and controls. Conclusions: Our results may be explained by the relatively small sample size.
- Innate immunity and inflammation in Alzheimer's disease pathogenesis(2017) TAKADA, Leonel Tadao
bookPart Afasias progressivas primárias(2021) TAKADA, Leonel Tadao