ORESTES VICENTE FORLENZA

(Fonte: Lattes)
Índice h a partir de 2011
39
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Psiquiatria, Faculdade de Medicina - Docente
LIM/27 - Laboratório de Neurociências, Hospital das Clínicas, Faculdade de Medicina

Resultados de Busca

Agora exibindo 1 - 10 de 228
  • conferenceObject
    Body awareness therapy reduces residual depressive symptoms in elderly subjects.
    (2012) COSTA, Ana Carolina O.; KAMKHAGI, Dorli; SUPINO, Deborah; KUSMISKY, Sandra; FORLENZA, Orestes V.; DINIZ, Breno S.
  • article 67 Citação(ões) na Scopus
    White matter abnormalities associated with Alzheimer's disease and mild cognitive impairment: a critical review of MRI studies
    (2013) RADANOVIC, Marcia; PEREIRA, Fabricio Ramos Silvestre; STELLA, Florindo; APRAHAMIAN, Ivan; FERREIRA, Luiz Kobuti; FORLENZA, Orestes Vicente; BUSATTO, Geraldo F.
    In this article, the authors aim to present a critical review of recent MRI studies addressing white matter (WM) abnormalities in Alzheimer's disease (AD) and mild cognitive impairment (MCI), by searching PubMed and reviewing MRI studies evaluating subjects with AD or MCI using WM volumetric methods, diffusion tensor imaging and assessment of WM hyperintensities. Studies have found that, compared with healthy controls, AD and MCI samples display WM volumetric reductions and diffusion tensor imaging findings suggestive of reduced WM integrity. These changes affect complex networks relevant to episodic memory and other cognitive processes, including fiber connections that directly link medial temporal structures and the corpus callosum. Abnormalities in cortico-cortical and cortico-subcortical WM interconnections are associated with an increased risk of progression from MCI to dementia. It can be concluded that WM abnormalities are detectable in early stages of AD and MCI. Degeneration of WM networks causes disconnection among neural cells and the degree of such changes is related to cognitive decline.
  • bookPart
    Delirium
    (2014) FORLENZA, Orestes Vicente; SANTOS, Franklin Santana
  • article 51 Citação(ões) na Scopus
    Neuropsychiatric symptoms in the prodromal stages of dementia
    (2014) STELLA, Florindo; RADANOVIC, Marcia; BALTHAZAR, Marcio L. F.; CANINEU, Paulo R.; SOUZA, Leonardo C. de; FORLENZA, Orestes V.
    Purpose of reviewTo critically discuss the neuropsychiatric symptoms in the prodromal stages of dementia in order to improve the early clinical diagnosis of cognitive and functional deterioration.Recent findingsCurrent criteria for cognitive syndrome, including Alzheimer's disease, comprise the neuropsychiatric symptoms in addition to cognitive and functional decline. Although there is growing evidence that neuropsychiatric symptoms may precede the prodromal stages of dementia, these manifestations have received less attention than traditional clinical hallmarks such as cognitive and functional deterioration. Depression, anxiety, apathy, irritability, agitation, sleep disorders, among other symptoms, have been hypothesized to represent a prodromal stage of dementia or, at least, they increase the risk for conversion from minor neurocognitive disorder to major neurocognitive disorder. Longitudinal investigations have provided increased evidence of progression to dementia in individuals with minor neurocognitive disorder when neuropsychiatric symptoms also were present.SummaryAlthough neuropsychiatric symptoms are strongly associated with a higher risk of cognitive and functional deterioration, frequently the clinician does not acknowledge these conditions as increasing the risk of dementia. When the clinician accurately diagnoses neuropsychiatric symptoms in the prodromal stage of dementia, he could early establish appropriate treatment and, may be, delay the beginning of clinical and functional deterioration.
  • conferenceObject
    Mixed mood states and optimizing generalizability: An update from the global aging & geriatric experiments in bipolar disorder database (GAGE-BD)
    (2021) SAJATOVIC, Martha; DOLS, Annemiek; REJ, Soham; BLUMBERG, Hilary; BRIGGS, Farren; FORESTER, Brent; FORLENZA, Orestes; GILDENGERS, Ariel; MULSANT, Benoit; SCHOUWS, Sigfried; SUTHERLAND, Ashley; TSAI, Shang-Ying; VIETA, Eduard; EYLER, Lisa
  • article 26 Citação(ões) na Scopus
    Cognitive Reserve Relates to Functional Network Efficiency in Alzheimer's Disease
    (2018) WEILER, Marina; CASSEB, Raphael Fernandes; CAMPOS, Brunno Machado de; TEIXEIRA, Camila Vieira de Ligo; CARLETTI-CASSANI, Ana Flavia Mac Knight; VICENTINI, Jessica Elias; MAGALHAES, Thamires Naela Cardoso; ALMEIRA, Debora Queiroz de; TALIB, Leda Leme; FORLENZA, Orestes Vicente; BALTHAZAR, Marcio Luiz Figueredo; CASTELLANO, Gabriela
    Alzheimer's disease (AD) is the most common form of dementia, with no means of cure or prevention. The presence of abnormal disease-related proteins in the population is, in turn, much more common than the incidence of dementia. In this context, the cognitive reserve (CR) hypothesis has been proposed to explain the discontinuity between pathophysiological and clinical expression of AD, suggesting that CR mitigates the effects of pathology on clinical expression and cognition. fMRI studies of the human connectome have recently reported that AD patients present diminished functional efficiency in resting-state networks, leading to a loss in information flow and cognitive processing. No study has investigated, however, whether CR modifies the effects of the pathology in functional network efficiency in AD patients. We analyzed the relationship between CR, pathophysiology and network efficiency, and whether CR modifies the relationship between them. Fourteen mild AD, 28 amnestic mild cognitive impairment (aMCI) due to AD, and 28 controls were enrolled. We used education to measure CR, cerebrospinal fluid (CSF) biomarkers to evaluate pathophysiology, and graph metrics to measure network efficiency. We found no relationship between CR and CSF biomarkers; CR was related to higher network efficiency in all groups; and abnormal levels of CSF protein biomarkers were related to more efficient networks in the AD group. Education modified the effects of tau-related pathology in the aMCI and mild AD groups. Although higher CR might not protect individuals from developing AD pathophysiology, AD patients with higher CR are better able to cope with the effects of pathology-presenting more efficient networks despite pathology burden. The present study highlights that interventions focusing on cognitive stimulation might be useful to slow age-related cognitive decline or dementia and lengthen healthy aging.
  • article 1 Citação(ões) na Scopus
    Evaluation of 10-minute post-injection 11C-PiB PET and its correlation with 18F-FDG PET in older adults who are cognitively healthy, mildly impaired, or with probable Alzheimer's disease
    (2022) CARNEIRO, Camila de Godoi; FARIA, Daniele de Paula; COUTINHO, Artur Martins; ONO, Carla Rachel; DURAN, Fabio Luis de Souza; COSTA, Naomi Antunes da; GARCEZ, Alexandre Teles; SILVEIRA, Paula Squarzoni da; FORLENZA, Orestes Vicente; BRUCKI, Sonia Maria Dozzi; NITRINI, Ricardo; FILHO, Geraldo Busatto; BUCHPIGUEL, Carlos Alberto
    Objective: Positron emission tomography (PET) allows in vivo evaluation of molecular targets in neurodegenerative diseases, such as Alzheimer's disease. Mild cognitive impairment is an intermediate stage between normal cognition and Alzheimer-type dementia. In vivo fibrillar amyloid-beta can be detected in PET using [11C]-labeled Pittsburgh compound B (11C-PiB). In contrast, [18F] fluoro-2-deoxy-d-glucose (18F-FDG) is a neurodegeneration biomarker used to evaluate cerebral glucose metabolism, indicating neuronal injury and synaptic dysfunction. In addition, early cerebral uptake of amyloid-PET tracers can determine regional cerebral blood flow. The present study compared early-phase 11C-PiB and 18F-FDG in older adults without cognitive impairment, amnestic mild cognitive impairment, and clinical diagnosis of probable Alzheimer's disease.Methods: We selected 90 older adults, clinically classified as healthy controls, with amnestic mild cognitive impairment, or with probable Alzheimer's disease, who underwent an 18F-FDG PET, early -phase 11C-PiB PET and magnetic resonance imaging. All participants were also classified as amyloid-positive or-negative in late-phase 11C-PiB. The data were analyzed using statistical parametric mapping.Results: We found that the probable Alzheimer's disease and amnestic mild cognitive impairment group had lower early-phase 11C-PiB uptake in limbic structures than 18F-FDG uptake. The images showed significant interactions between amyloid-beta status (negative or positive). However, early -phase 11C-PiB appears to provide different information from 18F-FDG about neurodegeneration.Conclusions: Our study suggests that early-phase 11C-PiB uptake correlates with 18F-FDG, irrespective of the particular amyloid-beta status. In addition, we observed distinct regional distribution patterns between both biomarkers, reinforcing the need for more robust studies to investigate the real clinical value of early-phase amyloid-PET imaging.
  • article 2 Citação(ões) na Scopus
    Brain PET amyloid and neurodegeneration biomarkers in the context of the 2018 NIA-AA research framework: an individual approach exploring clinical-biomarker mismatches and sociodemographic parameters (vol 45, pg 616, 2020)
    (2020) COUTINHO, Artur Martins; BUSATTO, Geraldo F.; PORTO, Fabio Henrique de Gobbi; FARIA, Daniele de Paula; ONO, Carla Rachel; GARCEZ, Alexandre Teles; SQUARZONI, Paula; DURAN, Fabio Luiz de Souza; OLIVEIRA, Maira Okada de; TRES, Eduardo Sturzeneker; BRUCKI, Sonia Maria Dozzi; FORLENZA, Orestes Vicente; NITRINI, Ricardo; BUCHPIGUEL, Carlos Alberto
  • article 155 Citação(ões) na Scopus
    Brief screening for mild cognitive impairment: validation of the Brazilian version of the Montreal cognitive assessment
    (2013) MEMORIA, Claudia M.; YASSUDA, Monica S.; NAKANO, Eduardo Y.; FORLENZA, Orestes V.
    Background The Montreal Cognitive Assessment (MoCA) is a brief cognitive schedule that has been developed for the screening of patients with Mild Cognitive Impairment (MCI). MCI is recognized as a high-risk state for Alzheimer's disease. The aim of the present study is to examine the reliability and validity of the Brazilian version of the MoCA test (MoCA-BR) in a sample of older individuals with at least 4?years of education. Methods The MoCA-BR was administered to 112 older adults who were classified into three diagnostic groups according to their cognitive state (Alzheimer's disease, n?=?28; MCI, n?=?43; normal controls, n?=?41). This procedure was based on clinical and neuropsychological data. The performance in the MoCA-BR was compared with the Mini-mental state examination (MMSE) and the Cambridge Cognitive Examination. Diagnostic accuracy was examined with the receiver operating characteristic (ROC) curve analyses. Results Cronbach's alpha for the MoCA-BR was 0.75. Temporal stability (retesting after 3?months) using intraclass correlation coefficient was 0.75 (p?
  • article 55 Citação(ões) na Scopus
    Lower Cerebrospinal Fluid Concentration of Brain-Derived Neurotrophic Factor Predicts Progression from Mild Cognitive Impairment to Alzheimer's Disease
    (2015) FORLENZA, Orestes Vicente; DINIZ, Breno Satler; TEIXEIRA, Antonio Lucio; RADANOVIC, Marcia; TALIB, Leda Leme; ROCHA, Natalia Pessoa; GATTAZ, Wagner Farid
    There is little information on the dynamics of BDNF in the CSF in the continuum between healthy aging, MCI and AD. We included 128 older adults (77 with amnestic MCI, 26 with AD and 25 healthy controls). CSF BDNF level was measured by ELISA assay, and AD biomarkers (A beta(42), T-Tau and P-Tau(181)) were measured using a Luminex xMAP assay. CSF BDNF levels were significantly reduced in AD subjects compared to MCI and healthy controls (p = 0.009). Logistic regression models showed that lower CSF BDNF levels (p = 0.008), lower CSF A beta(42) (p = 0.005) and lower MMSE scores (p = 0.007) are significantly associated with progression from MCI to AD. The present study adds strong evidence of the involvement of BDNF in the pathophysiology of neurodegenerative changes in AD. Interventions aiming to restore central neurotrophic support may represent future therapeutic targets to prevent or delay the progression from MCI to AD.