M
Michael T. Lin
Researcher at Cornell University
Publications - 59
Citations - 11332
Michael T. Lin is an academic researcher from Cornell University. The author has contributed to research in topics: Mitochondrial DNA & Long-term potentiation. The author has an hindex of 36, co-authored 59 publications receiving 10271 citations. Previous affiliations of Michael T. Lin include Memorial Sloan Kettering Cancer Center & Nova Southeastern University.
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Journal ArticleDOI
Alzheimer's APP mangles mitochondria.
Michael T. Lin,M. Flint Beal +1 more
TL;DR: New findings in humans examine how mitochondrial function declines during Alzheimer disease and how this decline is driven by age, disease and environmental factors.
Journal ArticleDOI
Synaptic activity reduces intraneuronal Aβ, promotes APP transport to synapses and protects against Aβ-related synaptic alterations
Davide Tampellini,Nawreen Rahman,Eduardo F. Gallo,Zhenyong Huang,Magali Dumont,Estibaliz Capetillo-Zarate,Tao Ma,Rong Zheng,Bao Lu,David M. Nanus,Michael T. Lin,Gunnar K. Gouras,Gunnar K. Gouras +12 more
TL;DR: It is demonstrated that synaptic activity promotes the transport of the amyloid precursor protein to synapses using live cell imaging, and that the protease neprilysin is involved in reduction of intraneuronal β-amyloid with synaptic activity.
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Neuroprotection by cyclodextrin in cell and mouse models of Alzheimer disease
TL;DR: In this article, the effects of cyclic oligosaccharide compounds (CDs) were examined in cell and mouse models of Alzheimer disease (AD) and showed neuroprotective effects of CD in a transgenic mouse model of AD.
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Coenzyme Q10 decreases amyloid pathology and improves behavior in a transgenic mouse model of Alzheimer's disease.
Magali Dumont,Khatuna Kipiani,Fangmin Yu,Elizabeth Wille,Maya Katz,Noel Y. Calingasan,Gunnar K. Gouras,Michael T. Lin,M. Flint Beal +8 more
TL;DR: Results show decreased pathology and improved behavior in transgenic AD mice treated with the naturally occurring antioxidant compound CoQ10, which is well tolerated in humans and may be promising for therapeutic trials in AD.
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Internalized Antibodies to the Aβ Domain of APP Reduce Neuronal Aβ and Protect against Synaptic Alterations
Davide Tampellini,Jordi Magrané,Reisuke H. Takahashi,Feng Li,Michael T. Lin,Claudia G. Almeida,Gunnar K. Gouras +6 more
TL;DR: Evidence is provided that treatment of AD mutant neuroblastoma cells or primary neurons with Aβ antibodies decreases levels of intracellular Aβ, and treatment with A β antibodies protects against synaptic alterations that occur in APP mutant neurons.