Results 121 to 130 of about 1,107,227 (284)

Changes in intracellular calcium and glutathione in astrocytes as the primary mechanism of amyloid neurotoxicity [PDF]

, 2003
Although the accumulation of the neurotoxic peptide {beta} amyloid ({beta}A) in the CNS is a hallmark of Alzheimer's disease, the mechanism of {beta}A neurotoxicity remains controversial.
Abramov, A.Y., Duchen, M.R., Canevari, L.   +2 more
core  

Unraveling Alzheimer’s: the promise of aducanumab, lecanemab, and donanemab

The Egyptian Journal of Neurology, Psychiatry and Neurosurgery
Alzheimer’s disease (AD) is a neurodegenerative condition that causes cognitive decline, memory loss, and reduced personal autonomy. The pathology of AD involves the aggregation of abnormal brain proteins, specifically beta-amyloid plaques and tau ...
Taha Basit Ameen, Syeda Naveera Kashif, Syed Muhammad Iraj Abbas, Kulsoom Babar, Syed Muhammad Sinaan Ali, Abdul Raheem   +5 more
doaj   +1 more source

Plasma Beta-Amyloid and Metabolic Biomarkers: Age- and Sex-Stratified Analyses Suggest Limited Population-Level Associations

Medicina
Background and Objectives: This study examined the relationships between plasma beta-amyloid levels and systemic inflammatory, thyroid, and lipid biomarkers using complementary analytical approaches in a cross-sectional cohort undergoing plasma OAβ and ...
Hyeokjun Yun, Bo Kyeung Jung, Jae Kyung Kim   +2 more
doaj   +1 more source

Targeting Hippocampal PTEN Suppresses Ferroptosis and Rescues Cognitive Decline in Alzheimer's Disease via Dual AKT/GSK3β/Nrf2 and AKT/STAT3 Axes

Advanced Science, EarlyView.
PTEN knockdown activates AKT phosphorylation, promoting Nrf2 nuclear translocation and STAT3 activation, which upregulates GPX4 and antioxidant enzymes HO‐1, SOD1, SOD2, and NQO1. These coordinated changes reduce lipid peroxidation and ROS, inhibit ferroptosis, and ultimately ameliorate cognitive impairment in APP/PS1 transgenic mice, highlighting a ...
Da‐Wei Wang, Meng‐Meng Liu, Yu‐Chen Zhao, Jia‐Yi Li, Wen Li, Xin Yu   +5 more
wiley   +1 more source

α‐Synuclein Forms Distinct Micelle‐Like Assemblies at Low Ionic Strengths

Advanced Science, EarlyView.
At high ionic strength, α‐synuclein forms diverse assemblies, including oligomers, fibrils, and condensates. Here, we show that at low ionic strength, α‐synuclein adopts a distinct, low‐abundance assembly state. These assemblies maintain a constant size above a critical concentration and do not coalesce, suggesting a micelle‐like organization ...
Sophie Hertel, Soumik Ray, Federica Saraceno, Giacomo Nisini, Georgia Nasi, Thomas Oliver Mason, Antonin Kunka, Effrosyni Agrimaki, Dannie Juul Olesen, Francesco Simone Ruggeri, Alexander K. Buell   +10 more
wiley   +1 more source

Supramolecular Degraders: An Emerging Paradigm in Targeted Protein Degradation

Advanced Science, EarlyView.
Dynamic supramolecular assembly reshapes targeted protein degradation by coordinating modular degrader construction, delivery, functional integration, and intracellular assembly or activation across proteasomal, endosomal–lysosomal, and autophagy–lysosomal pathways.
Kongjun Liu, Xue Yuan, Yan Zhou, Rui Yuan, Shaocheng Xie, Yong Chen, Peiyi Wang, Jianmei Gao, Qihai Gong   +8 more
wiley   +1 more source

Phase Separation, Material State, and Condensate Fate in Mammalian Autophagy

Advanced Science, EarlyView.
ABSTRACT Biomolecular phase separation has emerged as a key organizing principle in macroautophagy (hereafter autophagy). In mammalian cells, phase‐separated condensates not only serve as substrates for selective degradation, but also act as dynamic platforms for cargo recognition, signaling integration, and autophagosome assembly.
Yuanqiang Lin, Mingran Dai, Enyong Dai, Rui Kang, Daniel J. Klionsky, Daolin Tang, Yu Sun, Ningning Lv, Junnan Jiang   +8 more
wiley   +1 more source

The Effect of Amyloid Beta on Synapses

, 2019
Alzheimer's disease (AD) is a neurodegenerative disease that leads to cognitive deficits. The brain dysfunction in AD is marked by an increase in amyloid-beta, the protein responsible for plaque deposition in the brain.
Frediani, Gabrielle
core  

Brain amyloid β protein and memory disruption in Alzheimer’s disease

Neuropsychiatric Disease and Treatment, 2010
Weiming XiaCenter for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USAAbstract: The development of amyloid-containing neuritic plaques is an invariable characteristic of ...
Weiming Xia
doaj  

Early Spatial and Contextual Coding Deficits in Hippocampal CA1 Precede Performance Decline in an Alzheimer's Disease Model

Advanced Science, EarlyView.
Two‐photon calcium imaging in behaving 5xFAD mice reveals early CA1 coding deficits before behavioral decline. Task‐related place cell activity and splitter cell trajectory coding are impaired, with reduced retrospective dominance and greater prospective weighting.
Yimei Li, Mary Ann Go, Hualong Zhang, Robertas Aleksynas, Juliana Kim, Mingyang Gao, Seigfred Prado, Magdalena Sastre, Simon R. Schultz   +8 more
wiley   +1 more source