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Article ; Online: The longitudinal early-onset Alzheimer's disease study (LEADS): Advancing our understanding of Alzheimer's disease in individuals aged 40-64.

Wilcock, Donna M

Alzheimer's & dementia : the journal of the Alzheimer's Association

2023 Volume 19 Suppl 9, Page(s) S7

MeSH term(s)	Humans ; Alzheimer Disease/epidemiology ; Longitudinal Studies
Language	English
Publishing date	2023-11-27
Publishing country	United States
Document type	Editorial
ZDB-ID	2211627-8
ISSN	1552-5279 ; 1552-5260
ISSN (online)	1552-5279
ISSN	1552-5260
DOI	10.1002/alz.13568
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Zs.A 6316: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 540: Show issues

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Article ; Online: Soluble Biomarkers of Cerebrovascular Pathologies.

Foley, Kate E / Wilcock, Donna M

Stroke

2024 Volume 55, Issue 4, Page(s) 801–811

Abstract: Vascular contributions to cognitive impairment and dementia (VCID) is an all-encompassing term that describes cognitive impairment due to cerebrovascular origins. With the advancement of imaging and pathological studies, we now understand that VCID is ... ...

Abstract	Vascular contributions to cognitive impairment and dementia (VCID) is an all-encompassing term that describes cognitive impairment due to cerebrovascular origins. With the advancement of imaging and pathological studies, we now understand that VCID is often comorbid with Alzheimer disease. While researchers in the Alzheimer disease field have been working for years to establish and test blood-based biomarkers for Alzheimer disease diagnosis, prognosis, clinical therapy discovery, and early detection, blood-based biomarkers for VCID are in their infancy and also face challenges. VCID is heterogeneous, comprising many different pathological entities (ischemic, or hemorrhagic), and spatial and temporal differences (acute or chronic). This review highlights pathways that are aiding the search for sensitive and specific blood-based cerebrovascular dysfunction markers, describes promising candidates, and explains ongoing initiatives to discover blood-based VCID biomarkers.
MeSH term(s)	Humans ; Alzheimer Disease/diagnosis ; Dementia, Vascular/diagnosis ; Cognitive Dysfunction ; Biomarkers/metabolism
Chemical Substances	Biomarkers
Language	English
Publishing date	2024-03-25
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	80381-9
ISSN	1524-4628 ; 0039-2499 ; 0749-7954
ISSN (online)	1524-4628
ISSN	0039-2499 ; 0749-7954
DOI	10.1161/STROKEAHA.123.044172
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Zs.A 448: Show issues

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Article ; Online: Mechanisms of ARIA: is it time to focus on the unique immune environment of the neurovascular unit?

Foley, Kate E / Weekman, Erica M / Wilcock, Donna M

Molecular neurodegeneration

2023 Volume 18, Issue 1, Page(s) 76

MeSH term(s)	Humans ; Brain ; Cerebral Amyloid Angiopathy ; Alzheimer Disease ; Blood-Brain Barrier
Language	English
Publishing date	2023-10-20
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2244557-2
ISSN	1750-1326 ; 1750-1326
ISSN (online)	1750-1326
ISSN	1750-1326
DOI	10.1186/s13024-023-00667-8
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Article ; Online: Vascular Considerations for Amyloid Immunotherapy.

Foley, Kate E / Wilcock, Donna M

Current neurology and neuroscience reports

2022 Volume 22, Issue 11, Page(s) 709–719

Abstract: Purpose of review: Amyloid beta (Aβ) plaque accumulation is a hallmark pathology contributing to Alzheimer's disease (AD) and is widely hypothesized to lead to cognitive decline. Decades of research into anti-Aβ immunotherapies provide evidence for ... ...

Abstract	Purpose of review: Amyloid beta (Aβ) plaque accumulation is a hallmark pathology contributing to Alzheimer's disease (AD) and is widely hypothesized to lead to cognitive decline. Decades of research into anti-Aβ immunotherapies provide evidence for increased Aβ clearance from the brain; however, this is frequently accompanied by complicated vascular deficits. This article reviews the history of anti-Aβ immunotherapies and clinical findings and provides recommendations moving forward. Recent findings: In 20 years of both animal and human studies, anti-Aβ immunotherapies have been a prevalent avenue of reducing hallmark Aβ plaques. In both models and with different anti-Aβ antibody designs, amyloid-related imaging abnormalities (ARIA) indicating severe cerebrovascular compromise have been common and concerning occurrence. ARIA caused by anti-Aβ immunotherapy has been noted since the early 2000s, and the mechanisms driving it are still unknown. Recent approval of aducanumab comes with renewed urgency to consider vascular deficits caused by anti-Aβ immunotherapy.
MeSH term(s)	Animals ; Humans ; Amyloid beta-Peptides ; Plaque, Amyloid/drug therapy ; Plaque, Amyloid/pathology ; Alzheimer Disease/drug therapy ; Amyloidogenic Proteins ; Amyloid ; Immunotherapy/methods ; Immunologic Factors ; Disease Models, Animal
Chemical Substances	Amyloid beta-Peptides ; Amyloidogenic Proteins ; Amyloid ; Immunologic Factors
Language	English
Publishing date	2022-10-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2057363-7
ISSN	1534-6293 ; 1528-4042
ISSN (online)	1534-6293
ISSN	1528-4042
DOI	10.1007/s11910-022-01235-1
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Zs.A 5549: Show issues

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Article ; Online: Sex-based differences in effector cells of the adaptive immune system during Alzheimer's disease and related dementias.

Lutshumba, Jenny / Wilcock, Donna M / Monson, Nancy L / Stowe, Ann M

Neurobiology of disease

2023 Volume 184, Page(s) 106202

Abstract: Neurological conditions such as Alzheimer's disease (AD) and related dementias (ADRD) present with many challenges due to the heterogeneity of the related disease(s), making it difficult to develop effective treatments. Additionally, the progression of ... ...

Abstract	Neurological conditions such as Alzheimer's disease (AD) and related dementias (ADRD) present with many challenges due to the heterogeneity of the related disease(s), making it difficult to develop effective treatments. Additionally, the progression of ADRD-related pathologies presents differently between men and women. With two-thirds of the population affected with ADRD being women, ADRD has presented itself with a bias toward the female population. However, studies of ADRD generally do not incorporate sex-based differences in investigating the development and progression of the disease, which is detrimental to understanding and treating dementia. Additionally, recent implications for the adaptive immune system in the development of ADRD bring in new factors to be considered as part of the disease, including sex-based differences in immune response(s) during ADRD development. Here, we review the sex-based differences of pathological hallmarks of ADRD presentation and progression, sex-based differences in the adaptive immune system and how it changes with ADRD, and the importance of precision medicine in the development of a more targeted and personalized treatment for this devastating and prevalent neurodegenerative condition.
MeSH term(s)	Male ; Female ; Humans ; Alzheimer Disease/therapy ; Dementia/therapy ; Immune System
Language	English
Publishing date	2023-06-15
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106202
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Zs.A 4444: Show issues

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Article ; Online: Infectious hypothesis of Alzheimer disease.

Seaks, Charles E / Wilcock, Donna M

PLoS pathogens

2020 Volume 16, Issue 11, Page(s) e1008596

MeSH term(s)	Alzheimer Disease/complications ; Alzheimer Disease/pathology ; Alzheimer Disease/virology ; Dementia/complications ; Dementia/virology ; Herpesviridae/physiology ; Herpesviridae Infections/complications ; Herpesviridae Infections/pathology ; Herpesviridae Infections/virology ; Humans ; Plaque, Amyloid/complications ; Plaque, Amyloid/pathology ; Plaque, Amyloid/virology ; Protein Aggregates
Chemical Substances	Protein Aggregates
Language	English
Publishing date	2020-11-12
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1008596
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Article ; Online: The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer's Disease.

Kloske, Courtney M / Wilcock, Donna M

Frontiers in immunology

2020 Volume 11, Page(s) 754

Abstract: Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease, currently affecting over 5 million Americans with projections expected to rise as the population ages. The hallmark pathologies of AD are Aβ plaques composed of aggregated ... ...

Abstract	Alzheimer's disease (AD) is the most prevalent form of neurodegenerative disease, currently affecting over 5 million Americans with projections expected to rise as the population ages. The hallmark pathologies of AD are Aβ plaques composed of aggregated beta-amyloid (Aβ), and tau tangles composed of hyperphosphorylated, aggregated tau. These pathologies are typically accompanied by an increase in neuroinflammation as an attempt to ameliorate the pathology. This idea has pushed the field toward focusing on mechanisms and the influence neuroinflammation has on disease progression. The vast majority of AD cases are sporadic and therefore, researchers investigate genetic risk factors that could lead to AD. Apolipoprotein E (ApoE) is the largest genetic risk factor for developing AD. ApoE has 3 isoforms-ApoE2, ApoE3, and ApoE4. ApoE4 constitutes an increased risk of AD, with one copy increasing the risk about 4-fold and two copies increasing the risk about 15-fold compared to those with the ApoE3 allele. ApoE4 has been shown to play a role in Aβ deposition, tau tangle formation, neuroinflammation and many subsequent pathways. However, while we know that ApoE4 plays a role in these pathways and virtually all aspects of AD, the exact mechanism of how ApoE4 impacts AD progression is murky at best and therefore the role ApoE4 plays in these pathways needs to be elucidated. This review aims to discuss the current literature regarding the pathways and mechanisms of ApoE4 in AD progression with a focus on its role in neuroinflammation.
MeSH term(s)	Alzheimer Disease/etiology ; Amyloid beta-Peptides/metabolism ; Apolipoproteins E/physiology ; Astrocytes/physiology ; Autophagy ; Blood-Brain Barrier ; Humans ; Inflammation/etiology ; Signal Transduction ; tau Proteins/metabolism
Chemical Substances	Amyloid beta-Peptides ; Apolipoproteins E ; tau Proteins
Language	English
Publishing date	2020-04-30
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.00754
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Article ; Online: Pathologic sequelae of vascular cognitive impairment and dementia sheds light on potential targets for intervention.

Linton, Alexandria E / Weekman, Erica M / Wilcock, Donna M

Cerebral circulation - cognition and behavior

2021 Volume 2, Page(s) 100030

Abstract: Vascular contributions to cognitive impairment and dementia (VCID) is one of the leading causes of dementia along with Alzheimer's disease (AD) and, importantly, VCID often manifests as a comorbidity of AD(Vemuri and Knopman 2016; Schneider and Bennett ... ...

Abstract	Vascular contributions to cognitive impairment and dementia (VCID) is one of the leading causes of dementia along with Alzheimer's disease (AD) and, importantly, VCID often manifests as a comorbidity of AD(Vemuri and Knopman 2016; Schneider and Bennett 2010)(Vemuri and Knopman 2016; Schneider and Bennett 2010). Despite its common clinical manifestation, the mechanisms underlying VCID disease progression remains elusive. In this review, existing knowledge is used to propose a novel hypothesis linking well-established risk factors of VCID with the distinct neurodegenerative cascades of neuroinflammation and chronic hypoperfusion. It is hypothesized that these two synergistic signaling cascades coalesce to initiate aberrant angiogenesis and induce blood brain barrier breakdown trough a mechanism mediated by vascular growth factors and matrix metalloproteinases respectively. Finally, this review concludes by highlighting several potential therapeutic interventions along this neurodegenerative sequalae providing diverse opportunities for future translational study.
Language	English
Publishing date	2021-10-10
Publishing country	Netherlands
Document type	Journal Article
ISSN	2666-2450
ISSN (online)	2666-2450
DOI	10.1016/j.cccb.2021.100030
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Article ; Online: Neuroinflammatory phenotypes and their roles in Alzheimer's disease.

Wilcock, Donna M

Neuro-degenerative diseases

2014 Volume 13, Issue 2-3, Page(s) 183–185

Abstract: Background: Alzheimer's disease (AD) is characterized pathologically by the presence of amyloid plaques and neurofibrillary tangles in the brain. While once considered immunologically privileged due to the blood-brain barrier, it is now understood that ... ...

Abstract	Background: Alzheimer's disease (AD) is characterized pathologically by the presence of amyloid plaques and neurofibrillary tangles in the brain. While once considered immunologically privileged due to the blood-brain barrier, it is now understood that the glial cells of the brain are capable of complex inflammatory responses. Objective: The goal of the study is to assess the neuroinflammatory state of the early and late AD brain using the macrophage categorizations of M1, M2a, M2b and M2c. Methods: We used quantitative real-time RT-PCR to assess a number of inflammatory markers in the frontal cortex and cerebellar tissue from early and late AD patients. We then used neuropathological and clinical outcomes to determine whether there were any correlations. Results: We found that the AD brain is capable of generating all macrophage-like responses. In addition, we found that early AD is distinct from late AD with respect to the inflammatory profiles expressed in the brain. Most interestingly, however, we found that the early AD samples were biased to one of two phenotypes, M1 or M2a. Conclusion: Heterogeneity in the neuroinflammatory state of the early AD brain.
MeSH term(s)	Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Brain/pathology ; Cluster Analysis ; Female ; Humans ; Inflammation/genetics ; Inflammation/pathology ; Male ; Phenotype ; Real-Time Polymerase Chain Reaction ; Reverse Transcriptase Polymerase Chain Reaction ; Transcriptome
Language	English
Publishing date	2014
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2143569-8
ISSN	1660-2862 ; 1660-2854
ISSN (online)	1660-2862
ISSN	1660-2854
DOI	10.1159/000354228
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Zs.A 5918: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 567: Show issues

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Article ; Online: Using digital pathology to analyze the murine cerebrovasculature.

Niedowicz, Dana M / Gollihue, Jenna L / Weekman, Erica M / Phe, Panhavuth / Wilcock, Donna M / Norris, Christopher M / Nelson, Peter T

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism

2023 Volume 44, Issue 4, Page(s) 595–610

Abstract: Research on the cerebrovasculature may provide insights into brain health and disease. Immunohistochemical staining is one way to visualize blood vessels, and digital pathology has the potential to revolutionize the measurement of blood vessel parameters. ...

Abstract	Research on the cerebrovasculature may provide insights into brain health and disease. Immunohistochemical staining is one way to visualize blood vessels, and digital pathology has the potential to revolutionize the measurement of blood vessel parameters. These tools provide opportunities for translational mouse model research. However, mouse brain tissue presents a formidable set of technical challenges, including potentially high background staining and cross-reactivity of endogenous IgG. Formalin-fixed paraffin-embedded (FFPE) and fixed frozen sections, both of which are widely used, may require different methods. In this study, we optimized blood vessel staining in mouse brain tissue, testing both FFPE and frozen fixed sections. A panel of immunohistochemical blood vessel markers were tested (including CD31, CD34, collagen IV, DP71, and VWF), to evaluate their suitability for digital pathological analysis. Collagen IV provided the best immunostaining results in both FFPE and frozen fixed murine brain sections, with highly-specific staining of large and small blood vessels and low background staining. Subsequent analysis of collagen IV-stained sections showed region and sex-specific differences in vessel density and vessel wall thickness. We conclude that digital pathology provides a useful tool for relatively unbiased analysis of the murine cerebrovasculature, provided proper protein markers are used.
MeSH term(s)	Male ; Female ; Mice ; Animals ; Brain ; Collagen ; Paraffin Embedding
Chemical Substances	Collagen (9007-34-5)
Language	English
Publishing date	2023-11-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	604628-9
ISSN	1559-7016 ; 0271-678X
ISSN (online)	1559-7016
ISSN	0271-678X
DOI	10.1177/0271678X231216142
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