Journal ArticleDOI
Apoptosis is secondary to non-apoptotic axonal degeneration in neurons exposed to Aβ in distal axons
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TLDR
In agreement with previous suggestions that disruption of nerve growth factor (NGF)-mediated signaling might contribute to the loss of cholinergic neurons, it is found that provision of NGF to cell bodies protects sympathetic neurons from Abeta-induced apoptosis.About:
This article is published in Neurobiology of Aging.The article was published on 2006-09-01. It has received 43 citations till now. The article focuses on the topics: Calpain & Nerve growth factor.read more
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Human iPSC-Based Modeling of Late-Onset Disease via Progerin-Induced Aging
Justine D. Miller,Yosif Ganat,Sarah Kishinevsky,Robert L. Bowman,Becky Liu,Edmund Y. Tu,Pankaj Mandal,Pankaj Mandal,Elsa Vera,Jae-Won Shim,Sonja Kriks,Tony Taldone,Noemi Fusaki,Mark J. Tomishima,Dimitri Krainc,Teresa A. Milner,Teresa A. Milner,Derrick J. Rossi,Derrick J. Rossi,Lorenz Studer +19 more
TL;DR: It is suggested that progerin-induced aging can be used to reveal late-onset age-related disease features in hiPSC-based disease models.
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Resveratrol—A boon for treating Alzheimer's disease?
TL;DR: The role of resveratrol in modulating AD pathomechanisms is focused on and SIRT1, a human homologue of yeast silent information regulator (Sir)-2, and a member of NAD+-dependent histone deacetylases is found to be the prime mediator.
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Memantine protects rat cortical cultured neurons against beta-amyloid-induced toxicity by attenuating tau phosphorylation.
TL;DR: New insights are provided into the possible neuroprotective action of memantine against Aβ‐induced toxicity in Alzheimer’s disease brain.
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Axonal degeneration as a therapeutic target in the CNS
TL;DR: The evidence for axonal destruction from pathological findings and animal models with particular emphasis on neurodegenerative and neurotraumatic disorders is reviewed, and putative therapeutic targets based on the mechanistic prerequisites are concentrated.
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Internalization of β-Amyloid Peptide by Primary Neurons in the Absence of Apolipoprotein E *
TL;DR: It is demonstrated that Aβ-(1–42) is more efficiently internalized by axons than by cell bodies of sympathetic neurons, suggesting that A α7nAChR, previously suggested to be involved in Aβ internalization, is enriched in axons, which suggests an endocytic pathway involving caveolae/lipid rafts.
References
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Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo.
Dominic M. Walsh,Igor Klyubin,Julia V. Fadeeva,William K. Cullen,Roger Anwyl,Michael S. Wolfe,Michael J. Rowan,Dennis J. Selkoe +7 more
TL;DR: It is reported that natural oligomers of human Aβ are formed soon after generation of the peptide within specific intracellular vesicles and are subsequently secreted from the cell, indicating that synaptotoxic Aβ oligomers can be targeted therapeutically.
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Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction
Salvatore Oddo,Antonella Caccamo,Jason D. Shepherd,M. Paul Murphy,Todd E. Golde,Rakez Kayed,Raju Metherate,Mark P. Mattson,Yama Akbari,Frank M. LaFerla +9 more
TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.
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Caspase-12 mediates endoplasmic-reticulum-specific apoptosis and cytotoxicity by amyloid-beta.
TL;DR: It is shown that caspase-12 is localized to the ER and activated by ER stress, including disruption of ER calcium homeostasis and accumulation of excess proteins in ER, but not by membrane- or mitochondrial-targeted apoptotic signals, which may contribute to amyloid-β neurotoxicity.
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Neurotrophin signal transduction in the nervous system.
David R. Kaplan,Freda D. Miller +1 more
TL;DR: A number of novel p75NTR-interacting proteins have been identified that transmit growth, survival, and apoptotic signals.
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RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease
Shi Du Yan,Xi Chen,Jin Fu,Ming Chen,Huaijie Zhu,Alex E. Roher,Timothy Slattery,Lei Zhao,Mariko Nagashima,John Morser,Antonio Migheli,Peter P. Nawroth,David I. Stern,Ann Marie Schmidt +13 more
TL;DR: Evidence is presented that the 'receptor for advanced glycation end products' (RAGE) is such a receptor, and that it mediates effects of the peptide on neurons and microglia and indicates that it is relevant to the pathogenesis of neuronal dysfunction and death.