1,721,017 research outputs found
A new molecular explanation for age-related neurodegeneration: The Tyr682 residue of amyloid precursor protein
No full textNGF and APP Interplay: Focus on YENPTY Motif of Amyloid Precursor Protein and Y682 Residue
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Metabolic Syndrome and Autophagy: Focus on HMGB1 Protein
No full textMetabolic syndrome (MetS) affects the population worldwide and results from several factors such as genetic background, environment and lifestyle. In recent years, an interplay among autophagy, metabolism, and metabolic disorders has become apparent. Defects in the autophagy machinery are associated with the dysfunction of many tissues/organs regulating metabolism. Metabolic hormones and nutrients regulate, in turn, the autophagy mechanism. Autophagy is a housekeeping stress-induced degradation process that ensures cellular homeostasis. High mobility group box 1 (HMGB1) is a highly conserved nuclear protein with a nuclear and extracellular role that functions as an extracellular signaling molecule under specific conditions. Several studies have shown that HMGB1 is a critical regulator of autophagy. This mini-review focuses on the involvement of HMGB1 protein in the interplay between autophagy and MetS, emphasizing its potential role as a promising biomarker candidate for the early stage of MetS or disease’s therapeutic target
Apoptosis and in vitro Alzheimer disease neuronal models
No full textAlzheimer disease (AD) is a human neurodegenerative disease characterized by co-existence of extracellular senile plaques (SP) and neurofibrillary tangles (NFT) associated with an extensive neuronal loss, primarily in the cerebral cortex and hippocampus. Several studies suggest that caspase(s)-mediated neuronal death occurs in cellular and animal AD models as well as in human brains of affected patients, although an etiologic role of apoptosis in such neurodegenerative disorder is still debated. This review summarizes the experimental evidences corroborating the possible involvement of apoptosis in AD pathogenesis and discusses the usefulness of ad hoc devised in vitro approaches to study how caspase(s), amyloidogenic processing and tau metabolism might reciprocally interact leading to neuronal death
The Y682ENPTY687 motif of APP: Progress and insights toward a targeted therapy for Alzheimer's disease patients
No full textNGF and BDNF signaling control amyloidogenic route and Aβ production in hippocampal neurons
No full textCorrection: Might Fibroblasts from Patients with Alzheimer’s Disease Reflect the Brain Pathology? A Focus on the Increased Phosphorylation of Amyloid Precursor Protein Tyr682 Residue, (Brain Sci, (2021), 11, 103, 10.3390/brainsci1101010)
No full textIn the original article [1], there was a mistake in “Figure 3”. During the assembly of Figure 3, Western blot panels labeled with APPpTyr, APP, and β-actin were mistakenly used for familiar patients with AD, AD, and healthy controls. This error also affected the optical density analysis of the APPpTyr levels reported in Figure 1 and Figure 3B, where the values corresponding to Figure 3 needed to be replaced. In contrast, APP and β-actins optical density analyses were performed on the correct panels that are now reported in Figure 3 and did not require changes in the corresponding Figure 3C–E. Nonetheless, these errors did not influence the overall significance of the results, which remain consistent with those reported and discussed in this article. The corrected “Figure 1 and Figure 3” appear below. The authors apologize for any inconvenience caused and state that the scientific conclusions are unaffected. The original article has been updated
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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