Publikationen, an denen er mitarbeitet Brian J. Bacskai (26)

2022

  1. Accelerated amyloid angiopathy and related vascular alterations in a mixed murine model of Alzheimer´s disease and type two diabetes

    Fluids and Barriers of the CNS, Vol. 19, Núm. 1

2021

  1. Mitochondria-ER contacts and glucose: the powerhouse of Alzheimer's disease?

    Cell Calcium

2020

  1. Increased mitochondrial calcium levels associated with neuronal death in a mouse model of Alzheimer’s disease

    Nature Communications, Vol. 11, Núm. 1

2018

  1. In Vivo imaging of microglia with multiphoton microscopy

    Frontiers in Aging Neuroscience, Vol. 10, Núm. JUL

2017

  1. Progressive Neuronal Pathology and Synaptic Loss Induced by Prediabetes and Type 2 Diabetes in a Mouse Model of Alzheimer’s Disease

    Molecular Neurobiology, Vol. 54, Núm. 5, pp. 3428-3438

2013

  1. Four-dimensional microglia response to anti-Aβ treatment in APP/PS1xCX3CR1/GFP mice

    IntraVital, Vol. 2, Núm. 2, pp. e25693

  2. Rapid β-amyloid deposition and cognitive impairment after cholinergic denervation in APP/PS1 mice

    Journal of Neuropathology and Experimental Neurology, Vol. 72, Núm. 4, pp. 272-285

2012

  1. Reducing available soluble β-amyloid prevents progression of cerebral amyloid angiopathy in transgenic mice

    Journal of Neuropathology and Experimental Neurology, Vol. 71, Núm. 11, pp. 1009-1017

2011

  1. Cerebrovascular lesions induce transient β-amyloid deposition

    Brain

2010

  1. Antioxidants have a rapid and long-lasting effect on neuritic abnormalities in APP:PS1 mice

    Neurobiology of Aging, Vol. 31, Núm. 12, pp. 2058-2068

  2. Triflusal reduces dense-core plaque load, associated axonal alterations and inflammatory changes, and rescues cognition in a transgenic mouse model of Alzheimer's disease

    Neurobiology of Disease, Vol. 38, Núm. 3, pp. 482-491

2009

  1. Existing plaques and neuritic abnormalities in APP:PS1 mice are not affected by administration of the gamma-secretase inhibitor LY-411575

    Molecular Neurodegeneration, Vol. 4, Núm. 1

  2. Matrix metalloproteinase inhibition reduces oxidative stress associated with cerebral amyloid angiopathy in vivo in transgenic mice

    Journal of Neurochemistry, Vol. 109, Núm. 6, pp. 1636-1647

2008

  1. Rapid appearance and local toxicity of amyloid-β plaques in a mouse model of Alzheimer's disease

    Nature, Vol. 451, Núm. 7179, pp. 720-724

  2. Rapid microglial response around amyloid pathology after systemic anti-Aβ antibody administration in PDAPP mice

    Journal of Neuroscience, Vol. 28, Núm. 52, pp. 14156-14164

2007

  1. A limited role for microglia in antibody mediated plaque clearance in APP mice

    Neurobiology of Disease, Vol. 28, Núm. 3, pp. 286-292

  2. Age-dependent cerebrovascular dysfunction in Tg2576 transgenic mouse model of human cerebral amyloid angiopathy

    Journal of Cerebral Blood Flow and Metabolism

  3. Age-dependent cerebrovascular dysfunction in a transgenic mouse model of cerebral amyloid angiopathy

    Brain, Vol. 130, Núm. 9, pp. 2310-2319

  4. Antibody-mediated clearance of amyloid-β peptide from cerebral amyloid angiopathy revealed by quantitative in vivo imaging

    Journal of Neuroscience, Vol. 27, Núm. 8, pp. 1973-1980

  5. Curcumin labels amyloid pathology in vivo, disrupts existing plaques, and partially restores distorted neurites in an Alzheimer mouse model

    Journal of Neurochemistry, Vol. 102, Núm. 4, pp. 1095-1104