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Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic variability in autosomal dominant Alzheimer's disease.
Lloyd, Grace M; Trejo-Lopez, Jorge A; Xia, Yuxing; McFarland, Karen N; Lincoln, Sarah J; Ertekin-Taner, Nilüfer; Giasson, Benoit I; Yachnis, Anthony T; Prokop, Stefan.
Afiliación
  • Lloyd GM; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
  • Trejo-Lopez JA; Department of Neuroscience, University of Florida, Gainesville, FL, 32610, USA.
  • Xia Y; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
  • McFarland KN; Department of Pathology, University of Florida, Gainesville, FL, 32610, USA.
  • Lincoln SJ; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
  • Ertekin-Taner N; Department of Neuroscience, University of Florida, Gainesville, FL, 32610, USA.
  • Giasson BI; Center for Translational Research in Neurodegenerative Disease, University of Florida, Gainesville, FL, 32610, USA.
  • Yachnis AT; Department of Neurology, University of Florida, Gainesville, FL, 32610, USA.
  • Prokop S; McKnight Brain Institute, University of Florida, Gainesville, FL, 32610, USA.
Acta Neuropathol Commun ; 8(1): 31, 2020 03 12.
Article en En | MEDLINE | ID: mdl-32164763
The discovery of mutations associated with familial forms of Alzheimer's disease (AD), has brought imperative insights into basic mechanisms of disease pathogenesis and progression and has allowed researchers to create animal models that assist in the elucidation of the molecular pathways and development of therapeutic interventions. Position 717 in the amyloid precursor protein (APP) is a hotspot for mutations associated with autosomal dominant AD (ADAD) and the valine to isoleucine amino acid substitution (V717I) at this position was among the first ADAD mutations identified, spearheading the formulation of the amyloid cascade hypothesis of AD pathogenesis. While this mutation is well described in multiple kindreds and has served as the basis for the generation of widely used animal models of disease, neuropathologic data on patients carrying this mutation are scarce. Here we present the detailed clinical and neuropathologic characterization of an APP V717I carrier, which reveals important novel insights into the phenotypic variability of ADAD cases. While age at onset, clinical presentation and widespread parenchymal beta-amyloid (Aß) deposition are in line with previous reports, our case also shows widespread and severe cerebral amyloid angiopathy (CAA). This patient also presented with TDP-43 pathology in the hippocampus and amygdala, consistent with limbic predominant age-related TDP-43 proteinopathy (LATE). The APOE ε2/ε3 genotype may have been a major driver of the prominent vascular pathology seen in our case. These findings highlight the importance of neuropathologic examinations of genetically determined AD cases and demonstrate striking phenotypic variability in ADAD cases.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Encéfalo / Angiopatía Amiloide Cerebral / Precursor de Proteína beta-Amiloide / Placa Amiloide / Proteinopatías TDP-43 / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies Límite: Aged / Female / Humans Idioma: En Revista: Acta Neuropathol Commun Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Encéfalo / Angiopatía Amiloide Cerebral / Precursor de Proteína beta-Amiloide / Placa Amiloide / Proteinopatías TDP-43 / Enfermedad de Alzheimer Tipo de estudio: Prognostic_studies Límite: Aged / Female / Humans Idioma: En Revista: Acta Neuropathol Commun Año: 2020 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido