Amyloid beta-peptide (A beta) has been shown to activate the classical complement pathway in vitro. Here, we demonstrate that this interaction is fully capable of killing cells and damaging cellular processes in mixed hippocampal cultures from embryonic day 18 rat fetuses. Lactic acid dehydrogenase (LDH) release and morphologic changes were used to evaluate toxicity.
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ACS Nano
January 2025
Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, QLD 4072, Australia.
Type-2-diabetes is a metabolic disorder where misfolding and oligomerization of islet amyloid polypeptide (IAPP) around islet-β cells oligomerizes and participates in the pathology. The oligomeric stage is toxic but transitory and leads to the formation of mature amyloid fibrils. The pathological specifics of mature amyloid fibrils are poorly understood.
View Article and Find Full Text PDFRSC Med Chem
December 2024
Department of Medicinal Chemistry, National Institute of Pharmaceutical Education and Research Sector 67, S. A. S. Nagar Punjab 160062 India
Aberrant protein misfolding and accumulation is considered to be a major pathological pillar of neurodegenerative disorders, including Alzheimer's and Parkinson's diseases. Aggregation of amyloid-β (Aβ) peptide leads to the formation of toxic amyloid fibrils and is associated with cognitive dysfunction and memory loss in Alzheimer's disease (AD). Designing molecules that inhibit amyloid aggregation seems to be a rational approach to AD drug development.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, Raebareli Transit Campus, Bijnour-Sisendi Road, Sarojini Nagar, Lucknow, Uttar Pradesh, 226002, India.
Alzheimer's disease (AD) is a common neurodegenerative disease characterized by progressive memory loss and cognitive decline. The processes underlying the pathophysiology of AD are still not fully understood despite a great deal of research. Since mitochondrial dysfunction affects cellular energy metabolism, oxidative stress, and neuronal survival, it is becoming increasingly clear that it plays a major role in the development of AD.
View Article and Find Full Text PDFAlzheimers Dement
January 2025
Department of Neurology, Neurological Institute, Taipei Veterans General Hospital, Taipei, Taiwan.
Introduction: Plasma phosphorylated tau (p-tau) biomarkers have improved Alzheimer's disease (AD) diagnosis, but data from diverse Asian populations are limited. This study evaluated plasma p-tau217 and p-tau181 levels in Korean and Taiwanese populations.
Methods: All participants (n = 270) underwent amyloid positron emission tomography (PET) and blood tests.
Front Immunol
January 2025
College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan, China.
Alzheimer's disease (AD) is the most common neurodegenerative disorder, accounting for approximately 70% of dementia cases worldwide. Patients gradually exhibit cognitive decline, such as memory loss, aphasia, and changes in personality and behavior. Research has shown that mitochondrial dysfunction plays a critical role in the onset and progression of AD.
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