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Changes in Adsorption, Aggregation, and Diffusion Nature of Amyloid β on a Lipid Membrane in an Open System.
Langmuir
January 2025
Faculty of Science, Yamagata University, 1-4-12, Kojirakawa, Yamagata 990-8560, Japan.
The aggregation and accumulation of amyloid β 42 (Aβ42) peptides on the surface of brain cells is associated with Alzheimer's disease (AD); however, the underlying molecular mechanisms remain unclear. Herein, we used a unique brain-mimetic open system that continuously flows Aβ42 solution to analyze the initial aggregation and adsorptive nature of Aβ42 at physiological concentrations on the lipid membrane. The open system accelerated the adsorption and dimerization kinetics.
View Article and Find Full Text PDFUncovering the intricacies of IGF-1 in Alzheimer's disease: new insights from regulation to therapeutic targeting.
Inflammopharmacology
January 2025
Neuropharmacology Division, Department of Pharmacology, ISF College of Pharmacy, Moga, 142001, Punjab, India.
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of amyloid-β plaques and tau tangles, leading to cognitive decline and dementia. Insulin-like Growth Factor-1 (IGF-1) is similar in structure to insulin and is crucial for cell growth, differentiation, and regulating oxidative stress, synaptic plasticity, and mitochondrial function. IGF-1 exerts its physiological effects by binding to the IGF-1 receptor (IGF-1R) and activating PI3K/Akt pathway.
View Article and Find Full Text PDFDistinct Aggregation Behavior of -Terminally Truncated Aβ Over Aβ in the Presence of Zn(II).
ACS Chem Neurosci
January 2025
Department of Chemistry, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 34141, Republic of Korea.
The deposition of amyloid-β (Aβ) aggregates and metal ions within senile plaques is a hallmark of Alzheimer's disease (AD). Among the modifications observed in Aβ peptides, -terminal truncation at Phe4, yielding Aβ, is highly prevalent in AD-affected brains and significantly alters Aβ's metal-binding and aggregation profiles. Despite the abundance of Zn(II) in senile plaques, its impact on the aggregation and toxicity of Aβ remains unexplored.
View Article and Find Full Text PDFPolystyrene Nanoplastics Hitch-Hike the Gut-Brain Axis to Exacerbate Parkinson's Pathology.
ACS Nano
January 2025
Nanomedicine Center, The Great Bay Area National Institute for Nanotechnology Innovation, 136 Kaiyuan Avenue, Guangzhou 510700, China.
The neurological implications of micro- and nanoplastic exposure have recently come under scrutiny due to the environmental prevalence of these synthetic materials. Parkinson's disease (PD) is a major neurological disorder clinically characterized by intracellular Lewy-body inclusions and dopaminergic neuronal death. These pathological hallmarks of PD, according to Braak's hypothesis, are mediated by the afferent propagation of α synuclein (αS) via the enteric nervous system, or the so-called gut-brain axis.
View Article and Find Full Text PDFPrevious surgery for lumbar spinal stenosis and association with amyloidosis and heart failure - A Danish nationwide study.
Amyloid
January 2025
Department of Cardiology, Copenhagen, Denmark.
Introduction: Cardiac Amyloidosis (CA) is characterised by amyloid fibril deposits causing heart failure (HF). Lumbar spinal stenosis (LSS) is recognised as a potential red flag for CA, but the association remains underexplored in large-scale studies.
Methods: This nationwide registry-based cohort study in Denmark included subjects ≥60 years with a history of LSS surgery.
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