ArticleBiochimica et biophysica acta. Molecular basis of disease2018
Aβ truncated species: Implications for brain clearance mechanisms and amyloid plaque deposition.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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39 citing papers in PubMed, 74 citations in OpenAlex.
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- Bridging prion biology and Alzheimer's disease: from pathogenic seeds to precision therapeutics.Frontiers in molecular neuroscience · 2025Review
- Identification of isoAsp7-Aβ as a major Aβ variant in Alzheimer's disease, dementia with Lewy bodies and vascular dementia.Acta neuropathologica · 2024Article
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- Blood plasma biomarkers for Alzheimer's disease: Aβ1-42/1-40 vs. AβX-42/X-40.Clinical chemistry and laboratory medicine · 2024Article
- Amyloid β Proteoforms Elucidated by Quantitative LC/MS in the 5xFAD Mouse Model of Alzheimer's Disease.Journal of proteome research · 2023Article
- FDA-approved carbonic anhydrase inhibitors reduce amyloid β pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Mass Spectrometry Imaging in Alzheimer's Disease.Brain connectivity · 2023Article
- Structural polymorphism and cytotoxicity of brain-derived β-amyloid extracts.Protein science : a publication of the Protein Society · 2023Review
- Brain Region-Specific Differences in Amyloid-β Plaque Composition in 5XFAD Mice.Life (Basel, Switzerland) · 2023Article
- Matrix Development for the Detection of Phosphorylated Amyloid-β Peptides by MALDI-TOF-MS.Journal of the American Society for Mass Spectrometry · 2023Article
- Is plasma amyloid-β 1-42/1-40 a better biomarker for Alzheimer's disease than AβX-42/X-40?Fluids and barriers of the CNS · 2022Article
- An atlas of amyloid aggregation: the impact of substitutions, insertions, deletions and truncations on amyloid beta fibril nucleation.Nature communications · 2022Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Extensive parenchymal and vascular Aβ deposits are pathological hallmarks of Alzheimer's disease (AD). Besides classic full-length peptides, biochemical analyses of brain deposits have revealed high degree of Aβ heterogeneity likely resulting from the action of multiple proteolytic enzymes. In spite of the numerous studies focusing in Aβ, the relevance of N- and C-terminal truncated species for AD pathogenesis remains largely understudied. In the present work, using novel antibodies specifically recognizing Aβ species N-terminally truncated at position 4 or C-terminally truncated at position 34, we provide a clear assessment of the differential topographic localization of these species in AD brains and transgenic models. Based on their distinct solubility, brain N- and C-terminal truncated species were extracted by differential fractionation and identified via immunoprecipitation coupled to mass spectrometry analysis. Biochemical/biophysical studies with synthetic homologues further confirmed the different solubility properties and contrasting fibrillogenic characteristics of the truncated species composing the brain Aβ peptidome. Aβ C-terminal degradation leads to the production of more soluble fragments likely to be more easily eliminated from the brain. On the contrary, N-terminal truncation at position 4 favors the formation of poorly soluble, aggregation prone peptides with high amyloidogenic propensity and the potential to exacerbate the fibrillar deposits, self-perpetuating the amyloidogenic loop. Detailed assessment of the molecular diversity of Aβ species composing interstitial fluid and amyloid deposits at different disease stages, as well as the evaluation of the truncation profile during various pharmacologic approaches will provide a comprehensive understanding of the still undefined contribution of Aβ truncations to the disease pathogenesis and their potential as novel therapeutic targets.
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