Induced pluripotent stem cell (iPSC) line HUi001-A was reprogrammed from skin fibroblasts via non-integrating, virus free self-replicating RNA. Skin fibroblasts from an 81-year-old female Caucasian familial Alzheimer's disease patient of Volga German family carrying N141I mutation in the PSEN2 gene (familial AD4, clinical summary confirmed Alzheimer's disease) was obtained from the Coriell Institute (AG09908). Generated iPSCs were characterized and pluripotency was confirmed.
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http://dx.doi.org/10.1016/j.scr.2020.101892 | DOI Listing |
Hereditas
January 2025
The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, No. 182 Chunhui Road, Longmatan District, Luzhou, Sichuan, 646000, China.
Background: Alzheimer's disease (AD) is a prevalent neurodegenerative disorder, with antibody-mediated immune responses to infectious diseases agents potentially playing a decisive role in its pathophysiological process. However, the causal relationship between antibodies and AD remains unclear.
Methods: A two-sample Mendelian randomization (MR) analysis was conducted to investigate the causal link between antibody-mediated immune responses to infectious diseases agents and the risk of AD.
Alzheimers Res Ther
January 2025
Department of Bioengineering, University of California, San Diego, La Jolla, CA, 92093, USA.
Background: PSEN1, PSEN2, and APP mutations cause Alzheimer's disease (AD) with an early age at onset (AAO) and progressive cognitive decline. PSEN1 mutations are more common and generally have an earlier AAO; however, certain PSEN1 mutations cause a later AAO, similar to those observed in PSEN2 and APP.
Methods: We examined whether common disease endotypes exist across these mutations with a later AAO (~ 55 years) using hiPSC-derived neurons from familial Alzheimer's disease (FAD) patients harboring mutations in PSEN1, PSEN2, and APP and mechanistically characterized by integrating RNA-seq and ATAC-seq.
Sci Rep
January 2025
Stem Cells Technology Research Center, Shiraz University of Medical Sciences, Shiraz, Iran.
In this study, new cinnamic acid linked to triazole acetamide derivatives was synthesized and evaluated for anti-Alzheimer and anti-melanogenesis activities. The structural elucidation of all analogs was performed using different analytical techniques, including H-NMR, C-NMR, mass spectrometry, and IR spectroscopy. The synthesized compounds were assessed in vitro for their inhibitory activities against acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and tyrosinase enzymes.
View Article and Find Full Text PDFNat Cell Biol
January 2025
Department of Biochemistry and Molecular Biology, the Institute for Medical Research Israel-Canada, the Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
The protein homeostasis (proteostasis) network encompasses a myriad of mechanisms that maintain the integrity of the proteome by controlling various biological functions, including protein folding and degradation. Alas, ageing-associated decline in the efficiency of this network enables protein aggregation and consequently the development of late-onset neurodegenerative disorders, such as Alzheimer's disease. Accordingly, the maintenance of proteostasis through late stages of life bears the promise to delay the emergence of these devastating diseases.
View Article and Find Full Text PDFMikrochim Acta
January 2025
School of Pharmaceutical Sciences, Zhengzhou University, Zhengzhou, 450001, China.
A nano-enzyme sandwich assay (SWzyme assay), a colorimetric system based on a biochip and inorganic nano-enzyme for rapid and simple determination of exosomal Aβ42 in plasma is proposed. Anti-CD63 antibody-modified biochips were prepared for plasma exosome capture and synthesized highly catalytic Ni@Pt nanozymes for detecting exosomal Aβ42. The method was able to detect exosomal Aβ42 with a limit of detection (LOD) as low as 4.
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