Results 81 to 90 of about 1,190 (173)
Tauopathies as clinicopathological entities [PDF]
Tauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial inclusions composed of the microtubule-binding protein, tau. Several lines of evidence suggest tau aggregation is central to the neurodegenerative process in tauopathies.
openaire +2 more sources
This study investigates amyloid‐beta (Aβ) pathology in a forensic autopsy cohort of relatively young individuals (40–69 years). Using detailed immunohistochemical analyses of multiple Aβ species, we demonstrate marked regional and molecular heterogeneity, particularly within the striatum.
Shojiro Ichimata +4 more
wiley +1 more source
Background and Aim: Tau protein is a microtubule-associated protein that plays a critical role in microtubule dynamics and maintaining the structure of neurons.
Mohammad Majidi +2 more
doaj
Artificial intelligence–based 3D segmentation of tangle‐associated TDP‐43 in neurodegeneration
Multiplex immunostaining of anti‐phosphorylated TDP‐43, tau (AT8, pS396, TauC3, MN423, GT38), and Thioflavin S combined with AI‐based object recognition, reconstruction, and TAT maturation analysis pipeline in limbic regions revealed that distinct aggregation and tangle maturation patterns underscored region‐specific dynamics in the neurodegenerative ...
Gokhan Uruk +6 more
wiley +1 more source
Heritability in frontotemporal tauopathies
AbstractIntroductionExploring the degree of heritability in a large cohort of frontotemporal lobar degeneration with tau‐immunopositive inclusions (FTLD‐tau) and determining if different FTLD‐tau subtypes are associated with stronger heritability will provide important insight into disease pathogenesis.MethodsUsing modified Goldman pedigree ...
Shelley L. Forrest +9 more
openaire +3 more sources
Proteostasis of organelles in aging and disease
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Stimulating proteasomal degradation in human proteinopathies
The proteasome mediates the degradation of a wide range of proteins. Boosting proteasomal degradation may be beneficial in several disease contexts and can be achieved either by modulating proteasome activity or by improving substrate delivery. Proteasome activity can be enhanced by increasing proteasome abundance, inducing constitutive gate opening ...
Maria E. Gierisch +2 more
wiley +1 more source
Young adult deletion of microglial C1q reduced engulfment of Vglut1+ synapses and mitigated spatial cognitive deficits at 10 months of age in the amyloidopathy Arctic mouse model of AD. Neither fibrillar amyloid plaques nor soluble or insoluble Aβ levels in the hippocampus were affected by young adult microglial loss of C1q despite reduced phagocytosis
Tiffany J. Petrisko +4 more
wiley +1 more source
Elevated Plasma Phospho‐Tau217 in Beta‐Propeller Protein‐Associated Neurodegeneration
Movement Disorders, EarlyView.
Jae‐Hyeok Lee, Yun Soo Kim
wiley +1 more source
The in‐silico data showed that fisetin binds stably with the autophagy receptors and synaptic density regulators. Further, in‐vitro data confirmed the restoration of Aβ1‐42 disrupted autophagy by fisetin. Fisetin restored the oxidative stress and ion channels, along with a reduction of AChE activity.
Charu Jaiswal +2 more
wiley +1 more source

