The relative sensitivities of human fibroblast cultures from patients with familial Alzheimer's disease (AD), patients with Down's syndrome (Trisomy 21, T-21), and normal control (D-21) subjects, to the antiviral effect of human interferon-alpha (Hu-IFN-alpha) were compared. In confirmation of previous studies, T-21 cell lines showed significantly enhanced sensitivities to IFN compared with D-21 cells from normal controls. Fibroblast cultures from 2 familial AD patients belonging to one family exhibited sensitivities which fell within the range of response of normal D-21 cells. In contrast, fibroblasts from two other related subjects, one with familial AD and his niece "at risk", were extremely insensitive to interferon.

Download full-text PDF

Source
http://dx.doi.org/10.1007/BF01250054DOI Listing

Publication Analysis

Top Keywords

familial alzheimer's
8
alzheimer's disease
8
down's syndrome
8
human interferon-alpha
8
fibroblast cultures
8
d-21 cells
8
antiviral response
4
response fibroblasts
4
familial
4
fibroblasts familial
4

Similar Publications

Endoplasmic reticulum (ER) is a crucial organelle associated with cellular homeostasis. Accumulation of improperly folded proteins results in ER stress, accompanied by the reaction involving triggering unfolded protein response (UPR). The UPR is mediated through ER membrane-associated sensors, such as protein kinase-like ER kinase (PERK), inositol-requiring transmembrane kinase/endoribonuclease 1α, and activating transcription factor 6 (ATF6).

View Article and Find Full Text PDF

Natural products are ligands and in vitro inhibitors of Alzheimer's disease (AD) tau. Dihydromyricetin (DHM) bears chemical similarity to known natural product tau inhibitors. Despite having signature polyphenolic character, DHM is ostensibly hydrophobic owing to intermolecular hydrogen bonds that shield hydrophilic phenols.

View Article and Find Full Text PDF

α-Synucleinopathies constitute a spectrum of neurodegenerative disorders, including Parkinson's disease (PD), Lewy body dementia (LBD), Multiple System Atrophy (MSA), and Alzheimer's disease concurrent with LBD (AD-LBD). These disorders are unified by a pathological hallmark: aberrant misfolding and accumulation of α-synuclein (α-syn). This review delves into the pivotal role of α-syn, the key agent in α-synucleinopathy pathophysiology, and provides a survey of potential therapeutics that target cell-to-cell spread of pathologic α-syn.

View Article and Find Full Text PDF

Bone marrow mesenchymal stem cells derived cytokines associated with AKT/IAPs signaling ameliorate Alzheimer's disease development.

Stem Cell Res Ther

January 2025

NHC Key Laboratory of Human Disease Comparative Medicine, Beijing Engineering Research Center for Experimental Animal Models of Human Critical Diseases, International Center for Technology and Innovation of Animal Model, Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences (CAMS) & Comparative Medicine Center, Peking Union Medical College (PUMC), Beijing, 100021, China.

Background: Alzheimer's disease (AD) is a progressive neurodegenerative condition affecting around 50 million people worldwide. Bone marrow-derived mesenchymal stem cells (BMMSCs) have emerged as a promising source for cellular therapy due to their ability to differentiate into multiple cell types and their paracrine effects. However, the direct injection of BMMSCs can lead to potential unpredictable impairments, prompting a renewed interest in their paracrine effects for AD treatment.

View Article and Find Full Text PDF

A de novo, mosaic and complex chromosome 21 rearrangement causes APP triplication and familial autosomal dominant early onset Alzheimer disease.

Sci Rep

January 2025

Division for Neurogeriatrics, Centre for Alzheimer Research, Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Stockholm, Sweden.

Copy number variation (CNV) of the amyloid-β precursor protein gene (APP) is a known cause of autosomal dominant Alzheimer disease (ADAD), but de novo genetic variants causing ADAD are rare. We report a mother and daughter with neuropathologically confirmed definite Alzheimer disease (AD) and extensive cerebral amyloid angiopathy (CAA). Copy number analysis identified an increased number of APP copies and genome sequencing (GS) revealed the underlying complex genomic rearrangement (CGR) including a triplication of APP with two unique breakpoint junctions (BPJs).

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!