1. Arterial spin labeling imaging reveals widespread and Aβ-independent reductions in cerebral blood flow in elderly apolipoprotein epsilon-4 carriers.

    Journal of Cerebral Blood Flow and Metabolism 36(3):581 (2016) PMID 26661143 PMCID PMC4794091

    Changes in cerebral blood flow are an essential feature of Alzheimer's disease and have been linked to apolipoprotein E-genotype and cerebral amyloid-deposition. These factors could be interdependent or influence cerebral blood flow via different mechanisms. We examined apolipoprotein E-genotype...
  2. Regional cerebral blood flow estimated by early PiB uptake is reduced in mild cognitive impairment and associated with age in an amyloid-dependent manner.

    Neurobiology of Aging 36(4):1619 (2015) PMID 25702957

    Early uptake of [(11)C]-Pittsburgh Compound B (ePiB, 0-6 minutes) estimates cerebral blood flow. We studied ePiB in 13 PiB-negative and 10 PiB-positive subjects with mild cognitive impairment (MCI, n = 23) and 11 PiB-positive and 74 PiB-negative cognitively healthy elderly control subjects (HCS,...
  3. Posterior cingulate γ-aminobutyric acid and glutamate/glutamine are reduced in amnestic mild cognitive impairment and are unrelated to amyloid deposition and apolipoprotein E genotype.

    Neurobiology of Aging 36(1):53 (2015) PMID 25169676

    The biomarker potential of the inhibitory neurotransmitter γ-aminobutyric acid (GABA) for the in vivo characterization of preclinical stages in Alzheimer's disease has not yet been explored. We measured GABA, glutamate + glutamine (Glx), and N-acetyl-aspartate (NAA) levels by single-voxel MEGA-P...
  4. Volumetric and shape analysis of the thalamus and striatum in amnestic mild cognitive impairment.

    Journal of Alzheimer's Disease 49(1):237 (2015) PMID 26444755

    Alterations in brain structures, including progressive neurodegeneration, are a hallmark in patients with Alzheimer's disease (AD). However, pathological mechanisms, such as the accumulation of amyloid and the proliferation of tau, are thought to begin years, even decades, before the initial cli...

    Alzheimer's & Dementia 10(4):P826 (2014)


    Alzheimer's & Dementia 10(4):P548 (2014)


    Alzheimer's & Dementia 10(4):P713 (2014)

  8. Prefrontal brain network connectivity indicates degree of both schizophrenia risk and cognitive dysfunction.

    Schizophrenia Bulletin 40(3):653 (2014) PMID 23778975 PMCID PMC3984516

    Cognitive dysfunction is a core feature of schizophrenia, and persons at risk for schizophrenia may show subtle deficits in attention and working memory. In this study, we investigated the relationship between integrity of functional brain networks and performance in attention and working memory...
  9. Advances in active and passive immunotherapy for Alzheimer's disease

    Neurobiology of Aging 35:S10 (2014)

  10. Cortical Amyloid Beta in Cognitively Normal Elderly Adults is Associated with Decreased Network Efficiency within the Cerebro-Cerebellar System.

    Frontiers in Aging Neuroscience 6:52 (2014) PMID 24672483 PMCID PMC3957491

    Deposition of cortical amyloid beta (Aβ) is a correlate of aging and a risk factor for Alzheimer disease (AD). While several higher order cognitive processes involve functional interactions between cortex and cerebellum, this study aims to investigate effects of cortical Aβ deposition on couplin...
  11. Intraindividual variability across cognitive tasks as a potential marker for prodromal Alzheimer's disease.

    Frontiers in Aging Neuroscience 6:147 (2014) PMID 25071556 PMCID PMC4081834

    Recent studies have shown that increased cognitive intraindividual variability (IIV) across accuracy scores from tests representing different cognitive domains (across-domain IIV) might indicate prodromal Alzheimer's disease (AD). Although IIV has been proposed to index cognitive control process...
  12. Regional Fluid-Attenuated Inversion Recovery (FLAIR) at 7 Tesla correlates with amyloid beta in hippocampus and brainstem of cognitively normal elderly subjects.

    Frontiers in Aging Neuroscience 6:240 (2014) PMID 25249977 PMCID PMC4159032

    Accumulation of amyloid beta (Aβ) may occur during healthy aging and is a risk factor for Alzheimer Disease (AD). While individual Aβ-accumulation can be measured non-invasively using Pittsburgh Compund-B positron emission tomography (PiB-PET), Fluid-attenuated inversion recovery (FLAIR) is a Ma...
  13. Prefrontal executive function associated coupling relates to Huntington's disease stage

    Cortex 49(10):2661 (2013) PMID 23906595

    Huntington's disease (HD) is a neurodegenerative disease caused by cytosine–adenine–guanine (CAG)-repeat expansion in the huntingtin (HTT) gene. Early changes that may precede clinical manifestation of movement disorder include executive dysfunction. The aim of this study was to identi...
  14. Quantification of subcortical gray-matter vascularization using 7 Tesla time-of-flight angiography.

    Brain and Behavior 3(5):515 (2013) PMID 24392272 PMCID PMC3869979

    Background The integrity of subcortical brain nuclei is associated with maintenance of regular cognitive performance levels and has been shown to be particularly affected by aging-related vascular pathology. This study aims to demonstrate applicability of high field strength magnetic resonance a...
  15. Superresolution imaging of amyloid fibrils with binding-activated probes.

    ACS Chemical Neuroscience 4(7):1057 (2013) PMID 23594172 PMCID PMC3715833

    Protein misfolding into amyloid-like aggregates underlies many neurodegenerative diseases. Thus, insights into the structure and function of these amyloids will provide valuable information on the pathological mechanisms involved and aid in the design of improved drugs for treating amyloid-based...
  16. Visualization and quantification of APP intracellular domain-mediated nuclear signaling by bimolecular fluorescence complementation.

    PLoS ONE 8(9):e76094 (2013) PMID 24086696 PMCID PMC3783399

    The amyloid precursor protein (APP) intracellular domain (AICD) is released from full-length APP upon sequential cleavage by either α- or β-secretase followed by γ-secretase. Together with the adaptor protein Fe65 and the histone acetyltransferase Tip60, AICD forms nuclear multiprotein complexes...
  17. Deletion of the ageing gene p66(Shc) reduces early stroke size following ischaemia/reperfusion brain injury.

    European Heart Journal 34(2):96 (2013) PMID 23008506

    Stroke is a leading cause of morbidity and mortality, and its incidence increases with age. Both in animals and in humans, oxidative stress appears to play an important role in ischaemic stroke, with or without reperfusion. The adaptor protein p66(Shc) is a key regulator of reactive oxygen speci...
  18. Physical restraint use in nursing homes.

    JAMA 308(11):1091 (2012) PMID 22990262

  19. A novel mouse model of intraneuronal oligomers and congophilic amyloid angiopathy

    Alzheimer's & Dementia 8(4):P627 (2012)

  20. Intrapersonal variability as a cognitive marker of prodromal Alzheimer's disease

    Alzheimer's & Dementia 8(4):P352 (2012)