C-terminal peptides coassemble into A 42 oligomers and protect neurons against A 42-induced neurotoxicity
نویسندگان
چکیده
Departments of *Neurology and **Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, ††Brain Research Institute, and ¶¶Molecular Biology Institute, University of California, Los Angeles, CA 90095; §Center for Polymer Studies, Department of Physics, Boston University, Boston, MA 02215; and Center for Material Science and Engineering, Material Processing Center, and ‡‡Department of Physics, Massachusetts Institute of Technology, Cambridge, MA 02139
منابع مشابه
C-terminal fragments of APP: Its neurotoxic mechanisms and involvement in gene transcription
Several lines of evidence suggest that some neurotoxicity in AD is due to proteolytic fragments of APP. In this study, we compared the potency of neurotoxicity induced by CT with that of A-beta neurotoxicity and our results showed that various CT peptide fragments (CTFs; CTF99, AICD, CTF31) caused neurotoxicity in cultured cells and primary cortical neurons, induced strong non-selective inward ...
متن کاملC-terminal fragments of APP: Its neurotoxic mechanisms and involvement in gene transcription
Several lines of evidence suggest that some neurotoxicity in AD is due to proteolytic fragments of APP. In this study, we compared the potency of neurotoxicity induced by CT with that of A-beta neurotoxicity and our results showed that various CT peptide fragments (CTFs; CTF99, AICD, CTF31) caused neurotoxicity in cultured cells and primary cortical neurons, induced strong non-selective inward ...
متن کاملImpaired Memory and Evidence of Histopathology in CA1 Pyramidal Neurons through Injection of Aβ1-42 Peptides into the Frontal Cortices of Rat
Introduction: Alzheimer’s disease (AD) is one of the most common neurodegenerative disorders, which has much benefited from animal models to find the basics of its pathophysiology. In our previous work (Haghani, Shabani, Javan, Motamedi, & Janahmadi, 2012), a non-transgenic rat model of AD was used in electrophysiological studies. However, we did not investigate the histological aspects in the ...
متن کاملLack of neuroprotective effects by platelet-derived growth factor against beta-amyloid induced toxicity uncovers a novel hypothesis of Alzheimer's disease pathology
I hereby declare that I am the sole author of this thesis. This is a true copy of the thesis, including any required final revisions, as accepted by my examiners. I understand that my thesis may be made electronically available to the public. ABSTRACT Aβ oligomer-induced neurotoxicity has become an important area of therapeutic development in treating Alzheimer's disease. Platelet-derived growt...
متن کاملMitochondrial Ca2+ Overload Underlies Aβ Oligomers Neurotoxicity Providing an Unexpected Mechanism of Neuroprotection by NSAIDs
Dysregulation of intracellular Ca(2+) homeostasis may underlie amyloid beta peptide (Abeta) toxicity in Alzheimer's Disease (AD) but the mechanism is unknown. In search for this mechanism we found that Abeta(1-42) oligomers, the assembly state correlating best with cognitive decline in AD, but not Abeta fibrils, induce a massive entry of Ca(2+) in neurons and promote mitochondrial Ca(2+) overlo...
متن کامل