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.

Download full-text PDF

Source
http://dx.doi.org/10.1016/0304-3940(94)91088-xDOI Listing

Publication Analysis

Top Keywords

amyloid beta-peptide
8
enhanced cytotoxicity
4
cytotoxicity amyloid
4
beta-peptide complement
4
complement dependent
4
dependent mechanism
4
mechanism amyloid
4
beta-peptide beta
4
beta activate
4
activate classical
4

Similar Publications

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 PDF

Peptide-based amyloid-beta aggregation inhibitors.

RSC 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 PDF

Recent advancements in the understanding of the alterations in mitochondrial biogenesis in Alzheimer's disease.

Mol 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 PDF

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.

View Article and Find Full Text PDF

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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!