D. Wilcock

Charles D. Smith, D. Wilcock, D. Powell, 2013, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

Intracranial Injection of Gammagard, a Human IVIg, Modulates the Inflammatory Response of the Brain and Lowers Aβ in APP/PS1 Mice Along a Different Time Course than Anti-Aβ Antibodies

D. Wilcock, T. Sudduth, Abigail Greenstein, 2013, The Journal of Neuroscience.

Nitric oxide‐mediated regulation of β ‐amyloid clearance via alterations of MMP‐9/TIMP‐1

C. Colton, D. Wilcock, D. Wink, 2012, Journal of neurochemistry.

Hyperhomocysteinemia as a Risk Factor for Vascular Contributions to Cognitive Impairment and Dementia

D. Wilcock, E. Weekman, Brittani R. Price, 2018, Front. Aging Neurosci..

Blood Flow Deficits and Cerebrovascular Changes in a Dietary Model of Hyperhomocysteinemia

D. Wilcock, E. Abner, C. Norris, 2019, ASN neuro.

APOE-ε2 and APOE-ε4 correlate with increased amyloid accumulation in cerebral vasculature.

David W Fardo, Peter T Nelson, G. Jicha, 2013, Journal of neuropathology and experimental neurology.

Time course of neuropathological events in hyperhomocysteinemic amyloid depositing mice reveals early neuroinflammatory changes that precede amyloid changes and cerebrovascular events

D. Wilcock, E. Weekman, T. Sudduth, 2019, Journal of Neuroinflammation.

Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition

D. Wilcock, S. Johnson, E. Weekman, 2020, Journal of Neuroinflammation.

In aged human brains without detected neuritic amyloid plaques, the severity of NFT pathology, and APOE genotype, are each associated with non-neuritic A β plaques

Ela, Janna H. Neltner, G. Jicha, 2019 .

Amyloid-PET Levels in the Precuneus and Posterior Cingulate Cortices Are Associated with Executive Function Scores in Preclinical Alzheimer's Disease Prior to Overt Global Amyloid Positivity.

G. Jicha, R. E. El Khouli, B. Gold, 2022, Journal of Alzheimer's disease : JAD.

The usefulness and challenges of transgenic mouse models in the study of Alzheimer's disease.

D. Wilcock, 2010, CNS & neurological disorders drug targets.

β-amyloid deposition is shifted to the vasculature and memory impairment is exacerbated when hyperhomocysteinemia is induced in APP/PS1 transgenic mice

D. Wilcock, Holly M. Brothers, E. Weekman, 2014, Alzheimer's Research & Therapy.

Vascular Considerations for Amyloid Immunotherapy

D. Wilcock, Kate E. Foley, 2022, Current Neurology and Neuroscience Reports.

Neuroinflammatory Phenotypes and Their Roles in Alzheimer's Disease

D. Wilcock, 2013, Neurodegenerative Diseases.

Interaction of NG2+ glial progenitors and microglia/macrophages from the injured spinal cord

C. Colton, D. Wilcock, J. Wrathall, 2009, Glia.

Evaluation of Blood-Based Exosomes as Biomarkers for Aging-Related TDP-43 pathology

Virginia M. Y. Lee, D. Wilcock, P. Nelson, 2022, bioRxiv.

MarkVCID cerebral small vessel consortium: I. Enrollment, clinical, fluid protocols

Victoria J. Williams, M. Fornage, M. Albert, 2021, Alzheimer's & dementia : the journal of the Alzheimer's Association.

Amyloid Reduction by Amyloid-β Vaccination Also Reduces Mouse Tau Pathology and Protects from Neuron Loss in Two Mouse Models of Alzheimer's Disease

Nastaran Gharkholonarehe, Michael P Vitek, Carol A Colton, 2009, The Journal of Neuroscience.

Development of a protocol to assess within-subject, regional white matter hyperintensity changes in aging and dementia

Charles D. Smith, G. Jicha, A. Andersen, 2021, Journal of Neuroscience Methods.

Diffuse Amyloid-β Plaques, Neurofibrillary Tangles, and the Impact of APOE in Elderly Persons' Brains Lacking Neuritic Amyloid Plaques.

Janna H. Neltner, G. Jicha, D. Wilcock, 2018, Journal of Alzheimer's disease : JAD.

Neuroinflammation in Alzheimer’s disease; A source of heterogeneity and target for personalized therapy

D. Wilcock, Holly M. Brothers, H. Brothers, 2015, Neuroscience.

The roles of inflammation and immune mechanisms in Alzheimer's disease

M. Carrillo, J. Molinuevo, P. Cole, 2016, Alzheimer's & dementia.

Dynamic Complexity of the Microglial Activation Response in Transgenic Models of Amyloid Deposition: Implications for Alzheimer Therapeutics

D. Wilcock, A. Rojiani, D. Morgan, 2005, Journal of neuropathology and experimental neurology.

Aβ vaccination in combination with behavioral enrichment in aged beagles: effects on cognition, Aβ, and microhemorrhages

D. Wilcock, M. Murphy, E. Abner, 2017, Neurobiology of Aging.

Two-day radial-arm water maze learning and memory task; robust resolution of amyloid-related memory deficits in transgenic mice

D. Diamond, D. Wilcock, D. Morgan, 2006, Nature Protocols.

Time Course of the Development of Alzheimer-like Pathology in the Doubly Transgenic PS1+APP Mouse

James P. O'Callaghan, Dave Morgan, J. O'Callaghan, 2002, Experimental Neurology.

The Amygdala as a Locus of Pathologic Misfolding in Neurodegenerative Diseases

Bela G Nelson, Ela Patel, G. Jicha, 2018, Journal of neuropathology and experimental neurology.

Genetic knockout of myosin light chain kinase (MLCK210) prevents cerebral microhemorrhages and attenuates neuroinflammation in a mouse model of vascular cognitive impairment and dementia

D. Wilcock, L. V. Van Eldik, A. Bachstetter, 2019, GeroScience.

Proceedings from the Albert Charitable Trust Inaugural Workshop on white matter and cognition in aging

M. Fornage, S. Carmichael, J. Graff‐Radford, 2019, GeroScience.

Expanding the horizon of research into the pathogenesis of the white matter diseases: Proceedings of the 2021 Annual Workshop of the Albert Research Institute for White Matter and Cognition

Farzaneh A. Sorond, S. Carmichael, V. Hachinski, 2021, GeroScience.

Aging in Down Syndrome and the Development of Alzheimer's Disease Neuropathology.

C. Lemere, D. Wilcock, E. Head, 2015, Current Alzheimer research.

Down’s syndrome, neuroinflammation, and Alzheimer neuropathogenesis

D. Wilcock, W. Griffin, D. W. Reynolds, 2013, Journal of Neuroinflammation.

Water exchange rate across the blood‐brain barrier is associated with CSF amyloid‐β 42 in healthy older adults

Elayna R. Seago, Danny J. J. Wang, G. Jicha, 2021, Alzheimer's & dementia : the journal of the Alzheimer's Association.

Apolipoprotein E ε4/4 genotype limits response to dietary induction of hyperhomocysteinemia and resulting inflammatory signaling

D. Fardo, D. Wilcock, T. Bottiglieri, 2022, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

Infectious hypothesis of Alzheimer disease

D. Wilcock, Charles E Seaks, 2020, PLoS pathogens.

Loss of tau elicits axonal degeneration in a mouse model of Alzheimer's disease

D. Wilcock, M. Vitek, D. Laskowitz, 2010, Neuroscience.

Inflammatory Pathways Are Impaired in Alzheimer Disease and Differentially Associated With Apolipoprotein E Status.

D. Fardo, D. Wilcock, P. Nelson, 2021, Journal of neuropathology and experimental neurology.

Determining the role of IL-4 induced neuroinflammation in microglial activity and amyloid-β using BV2 microglial cells and APP/PS1 transgenic mice

D. Wilcock, E. Abner, M. Mendenhall, 2015, Journal of Neuroinflammation.

Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease

J. Hardy, D. Diamond, D. Wilcock, 2000, Nature.

A beta peptide vaccination prevents memory loss in an animal model of Alzheimer's disease.

J. Hardy, D. Diamond, D. Wilcock, 2000, Nature.

Activity of flurbiprofen and chemically related anti-inflammatory drugs in models of Alzheimer's disease

E. Ongini, D. Wilcock, L. Gasparini, 2005, Brain Research Reviews.

Progression of Amyloid Pathology to Alzheimer's Disease Pathology in an Amyloid Precursor Protein Transgenic Mouse Model by Removal of Nitric Oxide Synthase 2

Nastaran Gharkholonarehe, Michael P Vitek, Carol A Colton, 2008, The Journal of Neuroscience.

Lithium Treatment of APPSwDI/NOS2−/− Mice Leads to Reduced Hyperphosphorylated Tau, Increased Amyloid Deposition and Altered Inflammatory Phenotype

C. Colton, D. Wilcock, Joan G. Wilson, 2012, PloS one.

Intrahippocampal LPS injections reduce Aβ load in APP+PS1 transgenic mice

D. Wilcock, D. Morgan, M. Gordon, 2001, Neurobiology of Aging.

Dysregulation of Na+/K+ ATPase by amyloid in APP+PS1 transgenic mice

D. Wilcock, D. Morgan, M. Gordon, 2005, BMC Neuroscience.

Post-acquisition processing confounds in brain volumetric quantification of white matter hyperintensities

Charles D. Smith, Gregory A. Jicha, Ahmed A. Bahrani, 2019, Journal of Neuroscience Methods.

Aβ efflux impairment and inflammation linked to cerebrovascular accumulation of amyloid-forming amylin secreted from pancreas

Manuel F. Navedo, G. Jicha, C. Troakes, 2023, Communications Biology.

Mechanisms of [beta]-amyloid clearance by anti-a[beta] antibody therapy.

D. Wilcock, 2004 .

Immunotherapy, vascular pathology, and microhemorrhages in transgenic mice.

C. Colton, D. Wilcock, 2009, CNS & neurological disorders drug targets.

Anti-amyloid-beta immunotherapy in Alzheimer's disease: relevance of transgenic mouse studies to clinical trials.

C. Colton, D. Wilcock, 2008, Journal of Alzheimer's disease : JAD.

Mechanisms of ß-Amyloid Clearance by Anti-Aß Antibody Therapy

D. Wilcock, 2004 .

Activation of matrix metalloproteinases following anti-Aβ immunotherapy; implications for microhemorrhage occurrence

T. L. Taylor, C. Colton, D. Wilcock, 2011, Journal of Neuroinflammation.

Intracranial administration of deglycosylated C-terminal-specific antiA β antibody efficiently clears amyloid plaques without activating microglia in amyloid-depositing transgenic mice

Jan Grimm, Dave Morgan, J. Grimm, 2015 .

Down syndrome individuals with Alzheimer's disease have a distinct neuroinflammatory phenotype compared to sporadic Alzheimer's disease

F. Schmitt, D. Wilcock, M. Murphy, 2015, Neurobiology of Aging.

Noninvasive characterization of Alzheimer’s disease by circulating, cell-free messenger RNA next-generation sequencing

S. Quake, J. Brewer, M. Nerenberg, 2020, Science Advances.

Matrix Metalloproteinase in Blood-Brain Barrier Breakdown in Dementia.

D. Wilcock, E. Weekman, 2015, Journal of Alzheimer's disease : JAD.

Passive immunotherapy against Aβ in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage

D. Wilcock, A. Rojiani, D. Morgan, 2004, Journal of Neuroinflammation.

Intracranially Administered Anti-Αβ Antibodies Reduce β-Amyloid Deposition by Mechanisms Both Independent of and Associated with Microglial Activation

Dave Morgan, D. Wilcock, K. Ugen, 2003, The Journal of Neuroscience.

Intracranially administered anti-Abeta antibodies reduce beta-amyloid deposition by mechanisms both independent of and associated with microglial activation.

D. Wilcock, K. Ugen, D. Morgan, 2003, The Journal of neuroscience : the official journal of the Society for Neuroscience.

Number of Abeta inoculations in APP+PS1 transgenic mice influences antibody titers, microglial activation, and congophilic plaque levels.

D. Wilcock, K. Ugen, J. Hardy, 2001, DNA and cell biology.

The association of circulating amylin with β‐amyloid in familial Alzheimer's disease

J. Hardy, G. Jicha, R. Guerreiro, 2021, Alzheimer's & dementia.

White Matter Hyperintensity Regression: Comparison of Brain Atrophy and Cognitive Profiles with Progression and Stable Groups

Charles D. Smith, Christopher E. Bauer, G. Jicha, 2019, Brain sciences.

Pathologic sequelae of vascular cognitive impairment and dementia sheds light on potential targets for intervention

D. Wilcock, E. Weekman, Alexandria E. Linton, 2021, Cerebral circulation - cognition and behavior.

APOE-Mimetic Peptides Reduce Behavioral Deficits, Plaques and Tangles in Alzheimer’s Disease Transgenics

C. Colton, D. Wilcock, Judianne Davis, 2012, Neurodegenerative Diseases.

Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease

C. Colton, D. Wilcock, M. Vitek, 2009, Neuroscience.

Are inflammatory profiles the key to personalized Alzheimer's treatment?

D. Wilcock, Holly M. Brothers, H. Brothers, 2013, Neurodegenerative disease management.

Early Stage Drug Treatment That Normalizes Proinflammatory Cytokine Production Attenuates Synaptic Dysfunction in a Mouse Model That Exhibits Age-Dependent Progression of Alzheimer's Disease-Related Pathology

Janna H. Neltner, D. Wilcock, D. S. St. Clair, 2012, The Journal of Neuroscience.

Neuroinflammatory phenotype in early Alzheimer's disease

F. Schmitt, D. Wilcock, P. Nelson, 2013, Neurobiology of Aging.

Plasma amyloid beta, neurofilament light chain, and total tau in the Systolic Blood Pressure Intervention Trial (SPRINT)

D. Reboussin, F. Elahi, L. Launer, 2021, Alzheimer's & dementia : the journal of the Alzheimer's Association.

Amyloid-PET and White Matter Hyperintensities Have Independent Effects on Baseline Cognitive Function and Synergistic Effects on Longitudinal Executive Function

G. Jicha, R. E. El Khouli, B. Gold, 2023, Brain sciences.

Delayed diapedesis of CD8 T cells contributes to long-term pathology after ischemic stroke in male mice

Ann M. Stowe, E. Plautz, D. Wilcock, 2021, Brain, Behavior, and Immunity.

Exercise-linked FNDC5/irisin rescues synaptic plasticity and memory defects in Alzheimer’s models

F. Tovar-Moll, O. Arancio, D. Wilcock, 2019, Nature Medicine.

Targeting Astrocyte Signaling Alleviates Cerebrovascular and Synaptic Function Deficits in a Diet-Based Mouse Model of Small Cerebral Vessel Disease

D. Wilcock, D. Powell, P. Nelson, 2023, The Journal of Neuroscience.

Vascular Contributions to Cognitive Impairment and Dementia: Topical Review of Animal Models.

D. Wilcock, A. Hainsworth, J. Madigan, 2016, Stroke.

A Changing Perspective on the Role of Neuroinflammation in Alzheimer's Disease

D. Wilcock, 2012, International journal of Alzheimer's disease.

Phosphorylation Dynamics Regulate Hsp27-Mediated Rescue of Neuronal Plasticity Deficits in Tau Transgenic Mice

J. Rogers, E. Weeber, D. Wilcock, 2010, The Journal of Neuroscience.

Genetic expression changes and pathologic findings associated with hyperhomocysteinemia in human autopsy brain tissue

G. Jicha, D. Fardo, D. Wilcock, 2022, Alzheimer's & dementia.

Genetic knockout of myosin light chain kinase (MLCK210) prevents cerebral microhemorrhages and attenuates neuroinflammation in a mouse model of vascular cognitive impairment and dementia

D. Wilcock, L. V. Van Eldik, A. Bachstetter, 2019, GeroScience.

An emerging role of astrocytes in vascular contributions to cognitive impairment and dementia

D. Wilcock, C. Norris, P. Sompol, 2018, Journal of neurochemistry.

Hyperhomocysteinemia-Induced Gene Expression Changes in the Cell Types of the Brain

D. Wilcock, E. Weekman, T. Sudduth, 2017, ASN neuro.

APOE and immunity: Research highlights

Tyler J. Wishard, M. Carrillo, A. Brickman, 2023, Alzheimer's & dementia : the journal of the Alzheimer's Association.

White matter hyperintensities in vascular contributions to cognitive impairment and dementia (VCID): Knowledge gaps and opportunities

L. Beckett, H. Snyder, A. Brickman, 2019, Alzheimer's & dementia.

Therapeutic Trem2 activation ameliorates amyloid-beta deposition and improves cognition in the 5XFAD model of amyloid deposition

D. Wilcock, S. Johnson, E. Weekman, 2020, Journal of Neuroinflammation.

Neuroinflammation in the Aging Down Syndrome Brain; Lessons from Alzheimer's Disease

D. Wilcock, 2012, Current gerontology and geriatrics research.

Assessing activation states in microglia.

C. Colton, D. Wilcock, 2010, CNS & neurological disorders drug targets.

Vascular contributions to cognitive impairment and dementia (VCID).

D. Wilcock, M. Murphy, R. Corriveau, 2016, Biochimica et biophysica acta.

Association between APOE genotype and microglial cell morphology.

D. Wilcock, P. Nelson, E. Weekman, 2023, Journal of neuropathology and experimental neurology.

The contribution of inflammation to Alzheimer's disease in Down syndrome

D. Wilcock, E. Head, A. Martini, 2022, The Neurobiology of Aging and Alzheimer Disease in Down Syndrome.

Reduced Efficacy of Anti-Aβ Immunotherapy in a Mouse Model of Amyloid Deposition and Vascular Cognitive Impairment Comorbidity

D. Wilcock, D. Powell, E. Weekman, 2016, The Journal of Neuroscience.

Deglycosylated Anti-Amyloid-β Antibodies Eliminate Cognitive Deficits and Reduce Parenchymal Amyloid with Minimal Vascular Consequences in Aged Amyloid Precursor Protein Transgenic Mice

J. Grimm, D. Wilcock, J. Pons, 2006, The Journal of Neuroscience.

Microglial activation facilitates Aβ plaque removal following intracranial anti-Aβ antibody administration

D. Wilcock, K. Ugen, D. Morgan, 2004, Neurobiology of Disease.

Examining the association between blood‐based biomarkers and human post mortem neuropathology in the University of Kentucky Alzheimer's Disease Research Center autopsy cohort

Janna H. Neltner, G. Jicha, D. Wilcock, 2022, Alzheimer's & dementia : the journal of the Alzheimer's Association.

Animal Models of Vascular Cognitive Impairment and Dementia (VCID)

D. Wilcock, J. Gooch, 2016, Cellular and Molecular Neurobiology.

CSF and plasma placental growth factor as a biomarker for small‐vessel damage in VCID

G. Jicha, F. Elahi, D. Wilcock, 2021, Alzheimer's & Dementia.

Neurodegenerative pathologies associated with behavioral and psychological symptoms of dementia in a community-based autopsy cohort

F. Schmitt, G. Jicha, D. Fardo, 2023, Acta Neuropathologica Communications.

Microglial activation facilitates Abeta plaque removal following intracranial anti-Abeta antibody administration.

D. Wilcock, K. Ugen, D. Morgan, 2004, Neurobiology of disease.

Time course of neuropathological events in hyperhomocysteinemic amyloid depositing mice reveals early neuroinflammatory changes that precede amyloid changes and cerebrovascular events

D. Wilcock, E. Weekman, T. Sudduth, 2019, Journal of Neuroinflammation.

Amyloid-beta vaccination, but not nitro-nonsteroidal anti-inflammatory drug treatment, increases vascular amyloid and microhemorrhage while both reduce parenchymal amyloid.

D. Wilcock, D. Morgan, M. Gordon, 2007, Neuroscience.

Intracranial administration of Gammagard IVIg lowers amyloid and modulates neuroinflammatory profiles along a different time-course than anti-beta-amyloid IgG: Implications for mechanism of action

D. Wilcock, T. Sudduth, Abigail Greenstein, 2013, Alzheimer's & Dementia.

Apolipoprotein E proteinopathy is a major dementia-associated pathologic biomarker in individuals with or without the APOE epsilon 4 allele.

G. Jicha, D. Wilcock, M. Cykowski, 2021, The American journal of pathology.

A b peptide vaccination prevents memory loss in an animal model of Alzheimer ' s disease

D. Diamond, D. Wilcock, C. Hope, 2001 .

Evaluation of blood‐based, extracellular vesicles as biomarkers for aging‐related TDP‐43 pathology

Virginia M. Y. Lee, D. Wilcock, P. Nelson, 2022, Alzheimer's & dementia.

Global Cerebral Atrophy Detected by Routine Imaging: Relationship with Age, Hippocampal Atrophy, and White Matter Hyperintensities

Charles D. Smith, G. Jicha, B. Gold, 2018, Journal of neuroimaging : official journal of the American Society of Neuroimaging.

Plasma TDP‐43 levels are associated with neuroimaging measures of brain structure in limbic regions

Christopher E. Bauer, G. Jicha, B. Gold, 2023, Alzheimer's & dementia.

Review Article Vascular contributions to cognitive impairment and dementia including Alzheimer's disease

T. Montine, M. Carrillo, H. Snyder, 2014 .

correction: Aβ peptide vaccination prevents memory loss in an animal model of Alzheimer's disease

J. Hardy, D. Diamond, D. Wilcock, 2001, Nature.

Neurochemical studies of early-onset Alzheimerʼs disease

D. Neary, M. Esiri, N. Sims, 1987 .

Sanders-brown Center on Aging Faculty Publications Aging Transition from an M1 to a Mixed Neuroinflammatory Phenotype Increases Amyloid Deposition in App/ps1 Transgenic Mice Repository Citation Transition from an M1 to a Mixed Neuroinflammatory Phenotype Increases Amyloid Deposition in App/ps1 Trans

D. Wilcock, E. Abner, M. Mendenhall, 2022 .

Reduced efficacy of anti-Aβ immunotherapy in a mouse model of amyloid deposition and vascular cognitive impairment co-morbidity

D. Wilcock, E. Weekman, T. Sudduth, 2015, Alzheimer's & Dementia.

Common Pathogenic Mechanisms between Down Syndrome and Alzheimer's Disease: Steps toward Therapy

A. Granholm, F. Schmitt, D. Colas, 2018 .

EarlyStageDrugTreatmentThatNormalizes ProinflammatoryCytokineProductionAttenuatesSynaptic DysfunctioninaMouseModelThatExhibitsAge-Dependent ProgressionofAlzheimer'sDisease-RelatedPathology

D. Wilcock, C. Norris, A. Bachstetter, 2012 .

Activation of matrix metalloproteinases following antiA b immunotherapy ; implications for microhemorrhage occurrence

C. Colton, D. Wilcock, D. Wink, 2015 .

Intracranial administration of deglycosylated C-terminal-specific antiA β antibody efficiently clears amyloid plaques without activating microglia in amyloid-depositing transgenic mice

J. Grimm, D. Wilcock, J. Pons, 2015 .

D. Wilcock, E. Abner, M. Mendenhall, 2022 .

Lithium Treatment of APPSwDI/NOS22/2 Mice Leads to Reduced Hyperphosphorylated Tau, Increased Amyloid Deposition and Altered Inflammatory Phenotype

C. Colton, D. Wilcock, Joan G. Wilson, 2012 .

Passive immunotherapy against Aβ in aged APP-transgenic mice reverses cognitive deficits and depletes parenchymal amyloid deposits in spite of increased vascular amyloid and microhemorrhage

D. Wilcock, A. Rojiani, D. Morgan, 2004, Journal of Neuroinflammation.

Sanders-brown Center on Aging Faculty Publications Aging Lithium Treatment of Appswdi/nos2−/− Mice Leads to Reduced Hyperphosphorylated Tau, Increased Amyloid Deposition and Altered Inflammatory Phenotype Repository Citation Lithium Treatment of Appswdi/nos22/2 Mice Leads to Reduced Hyperphosphoryla

C. Colton, D. Wilcock, Joan G. Wilson, 2022 .

White matter hyperintensities influence distal cortical β-amyloid accumulation in default mode network pathways.

G. Jicha, R. E. El Khouli, B. Gold, 2023, Brain and behavior.

Reduced Efficacy of Anti-Aβ Immunotherapy in a Mouse Model of Amyloid Deposition and Vascular Cognitive Impairment Comorbidity

D. Wilcock, D. Powell, E. Weekman, 2016, The Journal of Neuroscience.

Induction of Hyperhomocysteinemia Models Vascular Dementia by Induction of Cerebral Microhemorrhages and Neuroinflammation

Charles D. Smith, D. Wilcock, D. Powell, 2013, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

Neuroinflammatory phenotype in early Alzheimer's disease

F. Schmitt, D. Wilcock, P. Nelson, 2013, Neurobiology of Aging.

Perspectives on ethnic and racial disparities in Alzheimer's disease and related dementias: Update and areas of immediate need

L. Schneider, H. Snyder, A. Brickman, 2018, Alzheimer's & Dementia.

Vascular amyloid alters astrocytic water and potassium channels in mouse models and humans with Alzheimer's disease

C. Colton, D. Wilcock, M. Vitek, 2009, Neuroscience.

Diverse inflammatory responses in transgenic mouse models of Alzheimer's disease and the effect of immunotherapy on these responses

C. Colton, D. Wilcock, Qun Zhao, 2011, ASN neuro.

Transition from an M1 to a mixed neuroinflammatory phenotype increases amyloid deposition in APP/PS1 transgenic mice

D. Wilcock, E. Abner, M. Mendenhall, 2014, Journal of Neuroinflammation.

Obesity and diabetes cause cognitive dysfunction in the absence of accelerated β-amyloid deposition in a novel murine model of mixed or vascular dementia

L. Hersh, N. Porter, D. Wilcock, 2014, Acta Neuropathologica Communications.

Homocysteine, hyperhomocysteinemia and vascular contributions to cognitive impairment and dementia (VCID).

D. Wilcock, A. Hainsworth, E. Weekman, 2016, Biochimica et biophysica acta.

Atorvastatin rescues hyperhomocysteinemia-induced cognitive deficits and neuroinflammatory gene changes

D. Fardo, D. Wilcock, T. Bottiglieri, 2023, Journal of Neuroinflammation.

β-amyloid deposition is shifted to the vasculature and memory impairment is exacerbated when hyperhomocysteinemia is induced in APP/PS1 transgenic mice

D. Wilcock, Holly M. Brothers, E. Weekman, 2014, Alzheimer's Research & Therapy.