2026-06-14T03:40:31Zhttps://repisalud.isciii.es/rest/oai/request
oai:repisalud.isciii.es:20.500.12105/184722024-11-28T14:42:35Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16927
Repisalud author de Oliveira, Jade author Kucharska, Ewa author Garcez, Michelle Lima author Rodrigues, Matheus Scarpatto author Quevedo, João author Moreno-Gonzalez, Ines author Budni, Josiane authoraffiliation [de Oliveira,J; Scarpatto Rodrigues,M] Programa de Pós-Graduação em Ciências Biológicas: Bioquímica, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.[Kucharska,E] Faculty of Education, Institute of Educational Sciences, Jesuit University Ignatianum in Krakow, Krakow, Poland. [Lima Garcez,M] Department of Biochemistry, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil. [Quevedo,J] Translational Psychiatry Program, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston. [Quevedo,J] Center of Excellence on Mood Disorders, Faillace Department of Psychiatry and Behavioral Sciences, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, USA. [Quevedo,J] Neuroscience Graduate Program, Graduate School of Biomedical Sciences, MD Anderson Cancer Center, UTHealth, The University of Texas Houston, Houston, TX, USA. [Quevedo,J] Graduate Program in Health Sciences, Translational Psychiatry Laboratory, University of Southern Santa Catarina (UNESC), Criciuma, Brazil. [Moreno-Gonzalez,I] Department of Cell Biology, Faculty of Sciences, University of Malaga, IBIMA, Malaga, Spain. [Moreno-Gonzalez,I] Networking Research Center on Neurodegenerative Diseases (CIBERNED), Malaga, Spain. [Moreno-Gonzalez,I] Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, USA. [Budni,J] Programa de Pós-Graduação em Ciências da Saúde, Laboratório de Neurologia Experimental, Universidade do Extremo Sul Catarinense, Criciuma, Brazil. 2024-02-19T15:31:33Z 2024-02-19T15:31:33Z 2021-09-28 10.3390/cells10102581 2073-4409 Cells http://hdl.handle.net/10668/3613 34685563 http://hdl.handle.net/20.500.12105/18472 Alzheimer's disease (AD) is the leading cause of dementia worldwide. Most AD patients develop the disease in late life, named late onset AD (LOAD). Currently, the most recognized explanation for AD pathology is the amyloid cascade hypothesis. It is assumed that amyloid beta (Aβ) aggregation and deposition are critical pathogenic processes in AD, leading to the formation of amyloid plaques, as well as neurofibrillary tangles, neuronal cell death, synaptic degeneration, and dementia. In LOAD, the causes of Aβ accumulation and neuronal loss are not completely clear. Importantly, the blood-brain barrier (BBB) disruption seems to present an essential role in the induction of neuroinflammation and consequent AD development. In addition, we propose that the systemic inflammation triggered by conditions like metabolic diseases or infections are causative factors of BBB disruption, coexistent inflammatory cascade and, ultimately, the neurodegeneration observed in AD. In this regard, the use of anti-inflammatory molecles could be an interesting strategy to treat, delay or even halt AD onset and progression. Herein, we review the inflammatory cascade and underlying mechanisms involved in AD pathogenesis and revise the anti-inflammatory effects of compounds as emerging therapeutic drugs against AD. eng Alzheimer’s disease Neurodegenerative disease Dementia Neuroinflammation Inflammatory cascade Systemic inflammation BBB disruption Anti-inflammatory effects Therapy Enfermedad de Alzheimer Enfermedades neurodegenerativas Demencia Terapéutica Síndrome de respuesta inflamatoria sistémica Inflammatory Cascade in Alzheimer's Disease Pathogenesis: A Review of Experimental Findings review article