Early long-term administration of the CSF1R inhibitor PLX3397 ablates microglia and reduces accumulation of intraneuronal amyloid, neuritic plaque deposition and pre-fibrillar oligomers in 5XFAD mouse model of Alzheimer’s disease

Autor: Justyna Sosna, Stephan Philipp, Ricardo Albay, Jorge Mauricio Reyes-Ruiz, David Baglietto-Vargas, Frank M. LaFerla, Charles G. Glabe

Publikováno v: Molecular Neurodegeneration, Vol 13, Iss 1, Pp 1-11 (2018)

Abstract Background Besides the two main classical features of amyloid beta aggregation and tau-containing neurofibrillary tangle deposition, neuroinflammation plays an important yet unclear role in the pathophysiology of Alzheimer’s disease (AD).

Externí odkaz: https://doaj.org/article/8db6198de3d844b4b96a4f34ba01cb0b

Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model

Autor: William C. Mobley, Ahmad Salehi, Cassia R. Overk, Y. Eugene Yu, Kim Weldy, Eric Doran, Ann Becker, Ricardo Albay, Mariko Sawa, Thomas G. Beach, Dominique Derse, Elizabeth Head

Publikováno v: Alzheimers Dement

Introduction People with Down syndrome (DS) are predisposed to Alzheimer's disease (AD). The amyloid hypothesis informs studies of AD. In AD-DS, but not sporadic AD, increased APP copy number is necessary, defining the APP gene dose hypothesis. Which

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3d2c8233805b6592ad881ea5f0583d05
https://pubmed.ncbi.nlm.nih.gov/34757693

Early long-term administration of the CSF1R inhibitor PLX3397 ablates microglia and reduces accumulation of intraneuronal amyloid, neuritic plaque deposition and pre-fibrillar oligomers in 5XFAD mouse model of Alzheimer's disease

Autor: Ricardo Albay, Frank M. LaFerla, Charles G. Glabe, Jorge Mauricio Reyes-Ruiz, David Baglietto-Vargas, Justyna Sosna, Stephan Philipp

Publikováno v: Molecular Neurodegeneration
Sosna, J; Philipp, S; III, AR; Reyes-Ruiz, JM; Baglietto-Vargas, D; LaFerla, FM; et al.(2018). Early long-term administration of the CSF1R inhibitor PLX3397 ablates microglia and reduces accumulation of intraneuronal amyloid, neuritic plaque deposition and pre-fibrillar oligomers in 5XFAD mouse model of Alzheimer's disease. MOLECULAR NEURODEGENERATION, 13. doi: 10.1186/s13024-018-0244-x. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/4vj8b7rz
Molecular Neurodegeneration, Vol 13, Iss 1, Pp 1-11 (2018)

Background Besides the two main classical features of amyloid beta aggregation and tau-containing neurofibrillary tangle deposition, neuroinflammation plays an important yet unclear role in the pathophysiology of Alzheimer’s disease (AD). Microglia

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::5202cc2944534f2d6ae817df3077b570
https://pubmed.ncbi.nlm.nih.gov/29490706

Intracellular amyloid and the neuronal origin of Alzheimer neuritic plaques

Autor: Lawrence Margol, Wayne W. Poon, Saskia Milton, Charles G. Glabe, Claudia H. Kawas, Suhail Rasool, Anna Pensalfini, Maria M. Corrada, Ricardo Albay, Asa Hatami, Hiromi Arai, Jessica W. Wu

Publikováno v: Pensalfini, A; Albay, R; Rasool, S; Wu, JW; Hatami, A; Arai, H; et al.(2014). Intracellular amyloid and the neuronal origin of Alzheimer neuritic plaques. Neurobiology of Disease, 71, 53-61. doi: 10.1016/j.nbd.2014.07.011. UC Irvine: Retrieved from: http://www.escholarship.org/uc/item/7n85j4v7
Neurobiology of Disease, Vol 71, Iss, Pp 53-61 (2014)

Genetic analysis of familial forms of Alzheimer's disease (AD) causally links the proteolytic processing of the amyloid precursor protein (APP) and AD. However, the specific type of amyloid and mechanisms of amyloid pathogenesis remain unclear. We co

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f490c2714691d379a1b6668d91729898
https://doi.org/10.1016/j.nbd.2014.07.011

Effective anti-Alzheimer Aβ therapy involves depletion of specific Aβ oligomer subtypes

Autor: Ricardo Albay, Soong Ho Kim, Norman R. Relkin, Elysse M. Knight, Sam Gandy, Jessica Kottwitz, Paul Szabo, Cristina M. Alberini, Akinobu Suzuki, William L. Klein, Alex L. Lublin, John W. Steele, Asa Hatami, Michelle E. Ehrlich, Charles G. Glabe

Publikováno v: Neurology® Neuroimmunology & Neuroinflammation

Background: Recent studies have implicated specific assembly subtypes of β-amyloid (Aβ) peptide, specifically soluble oligomers (soAβ) as disease-relevant structures that may underlie memory loss in Alzheimer disease. Removing existing soluble and

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9aaf9d9d5df2fc7a1006a61a0f83be75
http://europepmc.org/articles/PMC4864617