Eduardo Ferriolli
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Eduardo Ferriolli has a total of 13 co-authors. Here are the top co-authors by number of shared publications:
- Alberto Fernando Oliveira Justo
Division of Geriatrics, University of Sao Paulo Medical School, Brazil
1 shared publication - Antônio Lúcio Teixeira
University of Texas Health Science Center at San Antonio
1 shared publication - Carlos Augusto Pasqualucci
Department of Pathology, University of Sao Paulo Medical School, Brazil
1 shared publication - Claudia Kimie Suemoto
Division of Geriatrics, University of Sao Paulo Medical School, Brazil
1 shared publication - Eliana Cristina de Brito Toscano
Laboratório Integrado de Pesquisas em Patologia, Departamento de Patologia, Faculdade de Medicina Universidade Federal de Juiz de Fora Juiz de Fora Brazil
1 shared publication - Laura B. Grossi
Laboratory of Pathology, Department of Pathology, Federal University of Juiz de Fora Medical School, Juiz de Fora, Brazil
1 shared publication
Latest Publications
- 25 April 2025
- Published by Springer Nature in Molecular Neurobiology
- Vol. 62 (9) , 11348-11361
Upregulation of NLRP3 Inflammasome in Specific Hippocampal Regions: Strengthening the Link Between Neuroinflammation and Selective Vulnerability in Alzheimer’s Disease
Neuroinflammation has emerged as an important mechanism in the early stages of neurodegenerative diseases. Experimental models have demonstrated the detrimental role of inflammasomes in the development of Alzheimer’s disease (AD). However, neuropathological studies characterizing NLRP1 and NLRP3 pathways in AD are scarce. In addition, the possible association between inflammasome-induced neuroinflammation and clinicopathological outcomes is unclear. This study aimed to characterize the hippocampal expression of the inflammasome proteins in post-mortem samples of individuals with pure AD neuropathological change (ADNC) compared to controls from an admixed Latin American sample (n = 28 per group). We also investigated potential associations of inflammasome expression with neuropathological burden and cognitive abilities. The expression of NLRP1, NLRP3, caspase-1, ASC, gasdermin D, IL-1β, IL-18, amyloid β, and hyperphosphorylated tau (p-tau) was evaluated in the cornu ammonis (CA), dentate gyrus (DG), and subiculum (SUB), using immunohistochemistry and morphometry. We also performed the alignment of serial sections and 3D reconstruction of ADNC samples to verify the spatial locations of NLRP3/ASC and AD pathology across the hippocampus. We used ordinal logistic regression to investigate potential associations between inflammasome proteins and AD pathology, while linear regression assessed relationships between inflammasome and cognitive abilities. NLRP3, ASC, caspase-1, IL-1β, and IL-18 were overexpressed in CA and SUB of individuals with ADNC compared to controls. NLRP3 pathway correlated with AD pathology and CDR-SB, mainly in CA and SUB. Our results suggest that hippocampal NLRP3, but not NLRP1, inflammasome was associated with pathologic burden and cognitive impairment in AD and may contribute to the selective vulnerability to AD pathology.
- 25 April 2025
- Published by Springer Nature in Molecular Neurobiology
- Vol. 62 (9) , 11348-11361
Upregulation of NLRP3 Inflammasome in Specific Hippocampal Regions: Strengthening the Link Between Neuroinflammation and Selective Vulnerability in Alzheimer’s Disease
Neuroinflammation has emerged as an important mechanism in the early stages of neurodegenerative diseases. Experimental models have demonstrated the detrimental role of inflammasomes in the development of Alzheimer’s disease (AD). However, neuropathological studies characterizing NLRP1 and NLRP3 pathways in AD are scarce. In addition, the possible association between inflammasome-induced neuroinflammation and clinicopathological outcomes is unclear. This study aimed to characterize the hippocampal expression of the inflammasome proteins in post-mortem samples of individuals with pure AD neuropathological change (ADNC) compared to controls from an admixed Latin American sample (n = 28 per group). We also investigated potential associations of inflammasome expression with neuropathological burden and cognitive abilities. The expression of NLRP1, NLRP3, caspase-1, ASC, gasdermin D, IL-1β, IL-18, amyloid β, and hyperphosphorylated tau (p-tau) was evaluated in the cornu ammonis (CA), dentate gyrus (DG), and subiculum (SUB), using immunohistochemistry and morphometry. We also performed the alignment of serial sections and 3D reconstruction of ADNC samples to verify the spatial locations of NLRP3/ASC and AD pathology across the hippocampus. We used ordinal logistic regression to investigate potential associations between inflammasome proteins and AD pathology, while linear regression assessed relationships between inflammasome and cognitive abilities. NLRP3, ASC, caspase-1, IL-1β, and IL-18 were overexpressed in CA and SUB of individuals with ADNC compared to controls. NLRP3 pathway correlated with AD pathology and CDR-SB, mainly in CA and SUB. Our results suggest that hippocampal NLRP3, but not NLRP1, inflammasome was associated with pathologic burden and cognitive impairment in AD and may contribute to the selective vulnerability to AD pathology.