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The amyloid precursor protein and its derived fragments concomitantly contribute to the alterations of mitochondrial transport machinery in Alzheimer's disease.
- Published in:
- Cell Death & Disease, 2024, v. 15, n. 5, p. 1, doi. 10.1038/s41419-024-06742-2
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- Article
Potentially Pathogenic SORL1 Mutations Observed in Autosomal-Dominant Cases of Alzheimer's Disease Do Not Modulate APP Physiopathological Processing.
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- Cells (2073-4409), 2023, v. 12, n. 24, p. 2802, doi. 10.3390/cells12242802
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- Article
Correction to: Intraneuronal aggregation of the β‑CTF fragment of APP (C99) induces Aβ‑independent lysosomal-autophagic pathology.
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- 2023
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- Correction Notice
The η-secretase-derived APP fragment ηCTF is localized in Golgi, endosomes and extracellular vesicles and contributes to Aβ production.
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- Cellular & Molecular Life Sciences, 2023, v. 80, n. 4, p. 1, doi. 10.1007/s00018-023-04737-4
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- Article
Accumulation of amyloid precursor protein C-terminal fragments triggers mitochondrial structure, function, and mitophagy defects in Alzheimer's disease models and human brains.
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- Acta Neuropathologica, 2021, v. 141, n. 1, p. 39, doi. 10.1007/s00401-020-02234-7
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- Article
Post-translational remodeling of ryanodine receptor induces calcium leak leading to Alzheimer's disease-like pathologies and cognitive deficits.
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- Acta Neuropathologica, 2017, v. 134, n. 5, p. 749, doi. 10.1007/s00401-017-1733-7
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- Article
Genome-wide, high-content siRNA screening identifies the Alzheimer's genetic risk factor FERMT2 as a major modulator of APP metabolism.
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- Acta Neuropathologica, 2017, v. 133, n. 6, p. 955, doi. 10.1007/s00401-016-1652-z
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- Article
MT5-MMP Promotes Alzheimer's Pathogenesis in the Frontal Cortex of 5xFAD Mice and APP Trafficking in vitro.
- Published in:
- Frontiers in Molecular Neuroscience, 2017, v. 9, p. 1, doi. 10.3389/fnmol.2016.00163
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- Article
Aβ42 oligomers modulate β-secretase through an XBP-1s-dependent pathway involving HRD1.
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- Scientific Reports, 2016, p. 37436, doi. 10.1038/srep37436
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- Article
Intraneuronal aggregation of the β-CTF fragment of APP (C99) induces Aβ-independent lysosomal-autophagic pathology.
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- Acta Neuropathologica, 2016, v. 132, n. 2, p. 257, doi. 10.1007/s00401-016-1577-6
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- Publication type:
- Article
Mit RFID zu besserem Service und neuen Strukturen - das Beispiel UB Leipzig.
- Published in:
- Bibliotheksdienst, 2016, v. 50, n. 6, p. 545, doi. 10.1515/bd-2016-0063
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- Publication type:
- Article
MT5-MMP is a new pro-amyloidogenic proteinase that promotes amyloid pathology and cognitive decline in a transgenic mouse model of Alzheimer's disease.
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- Cellular & Molecular Life Sciences, 2016, v. 73, n. 1, p. 217, doi. 10.1007/s00018-015-1992-1
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- Article
Parkin acts as a transcription factor modulating presenilin-1 and presenilin-2 promoter transactivations.
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- 2013
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- Abstract
Parkin differently regulates presenilin-1 and presenilin-2 functions by direct control of their promoter transcription.
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- Journal of Molecular Cell Biology, 2013, v. 5, n. 2, p. 132, doi. 10.1093/jmcb/mjt003
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- Publication type:
- Article
The β-Secretase-Derived C-Terminal Fragment of βAPP, C99, But Not Aβ, Is a Key Contributor to Early Intraneuronal Lesions in Triple-Transgenic Mouse Hippocampus.
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- Journal of Neuroscience, 2012, v. 32, n. 46, p. 16243, doi. 10.1523/JNEUROSCI.2775-12.2012
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- Article
γ-Secretase-Mediated Regulation of Neprilysin: Influence of Cell Density and Aging and Modulation by Imatinib.
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- Journal of Alzheimer's Disease, 2011, v. 27, n. 3, p. 511, doi. 10.3233/JAD-2011-110746
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- Article