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Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases
Treatments targeting basic mitochondrial processes, such as energy metabolism or free-radical generation, or specific interactions of disease-related proteins with mitochondria hold great promise in ageing-related neurodegenerative diseases.
Beta-amyloid accumulation in APP mutant neurons reduces PSD-95 and GluR1 in synapses
Behavioral deficits and progressive neuropathology in progranulin-deficient mice: a mouse model of frontotemporal dementia.
- F. Yin, M. Dumont, A. Ding
- Biology, PsychologyFASEB journal : official publication of the…
- 1 December 2010
It is shown that progranulin-deficient mice displayed increased depression- and disinhibition-like behavior, as well as deficits in social recognition from a relatively young age, and these mice may serve as an important tool for deciphering underlying mechanisms in frontotemporal dementia.
Oligomerization of Alzheimer's β-Amyloid within Processes and Synapses of Cultured Neurons and Brain
It is demonstrated that primary neurons from Tg2576 mice recapitulate the in vivo localization and accumulation of Aβ42 with time in culture, and that A β42 aggregates into oligomers within endosomal vesicles and along microtubules of neuronal processes, which are associated with pathological alterations within processes and synaptic compartments in Tg 2576 mouse and human AD brains.
Increased plaque burden in brains of APP mutant MnSOD heterozygous knockout mice
Complete deficiency of MnSOD, which is well established to cause elevated oxidative stress, significantly increased brain Aβ levels and Aβ plaque burden in Tg19959 mice, indicating that oxidative stress can promote the pathogenesis of AD and support the feasibility of antioxidant approaches for AD therapy.
Internalized antibodies to the Abeta domain of APP reduce neuronal Abeta and protect against synaptic alterations.
Evidence is provided that treatment of AD mutant neuroblastoma cells or primary neurons with Abeta antibodies decreases levels of intracellular Abeta, and treatment with Abetas protects against synaptic alterations that occur in APP mutant neurons.
Dysregulation of the mTOR Pathway Mediates Impairment of Synaptic Plasticity in a Mouse Model of Alzheimer's Disease
Evidence is provided that inhibition of mTOR signaling correlates with impairment in synaptic plasticity in hippocampal slices from an AD mouse model and in wild-type slices exposed to exogenous Aβ1-42, which supports the notion that the mTOR pathway modulates Aβ-related synaptic dysfunction in AD.
Neuroprotection by cyclodextrin in cell and mouse models of Alzheimer disease
- Jiaqi Yao, Daniel Ho, N. Calingasan, N. Pipalia, Michael T. Lin, M. Beal
- BiologyThe Journal of experimental medicine
- 17 December 2012
To be added
Effects of Synaptic Modulation on β-Amyloid, Synaptophysin, and Memory Performance in Alzheimer's Disease Transgenic Mice
- D. Tampellini, E. Capetillo-Zarate, G. Gouras
- Biology, PsychologyThe Journal of Neuroscience
- 27 October 2010
It is shown that reduced synaptic activity causes detrimental effects on synapses and memory despite reducing plaques despite reduced plaques using two different models of chronic synaptic inhibition: deafferentation of the barrel cortex and administration of benzodiazepine.
The diagnostic utility of FLAIR imaging in clinically verified amyotrophic lateral sclerosis
- Lijuan Zhang, A. Uluğ, R. Zimmerman, Michael T. Lin, M. Rubin, M. Beal
- Psychology, MedicineJournal of magnetic resonance imaging : JMRI
- 1 May 2003
To explore the overall diagnostic ability of magnetic resonance (MR) fluid‐attenuated inversion recovery (FLAIR) imaging for clinically verified amyotrophic lateral sclerosis (ALS).