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  1. Article ; Online: Evaluating when (and how) hypertension may be 'good for your brain'.

    Magaki, Shino D / Vinters, Harry V

    Brain communications

    2023  Volume 5, Issue 2, Page(s) fcad127

    Abstract: This scientific commentary refers to 'Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation, at the expense of cerebral vascular damage', by ... ...

    Abstract This scientific commentary refers to 'Elevated late-life blood pressure may maintain brain oxygenation and slow amyloid-β accumulation, at the expense of cerebral vascular damage', by Tayler
    Language English
    Publishing date 2023-04-18
    Publishing country England
    Document type Journal Article
    ISSN 2632-1297
    ISSN (online) 2632-1297
    DOI 10.1093/braincomms/fcad127
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The 'ACCIDENTAL NEUROPATHOLOGIST'-PERSPECTIVES on 40 years in Neuropathology.

    Vinters, Harry V

    Free neuropathology

    2020  Volume 1

    Language English
    Publishing date 2020-08-25
    Publishing country Canada
    Document type Journal Article
    ISSN 2699-4445
    ISSN (online) 2699-4445
    DOI 10.17879/freeneuropathology-2020-2956
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book: Diagnostic neuropathology

    Vinters, Harry V.

    (Diagnostic pathology ; 1)

    1998  

    Author's details Harry V. Vinters
    Series title Diagnostic pathology ; 1
    Collection
    Language English
    Size IX, 669 S. : Ill.
    Publisher Dekker
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT012819221
    ISBN 0-8247-9888-0 ; 978-0-8247-9888-8
    Database Catalogue ZB MED Medicine, Health

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  4. Article ; Online: Neuropathologic Findings in Chronic Kidney Disease (CKD).

    Vinters, Harry V / Magaki, Shino D / Williams, Christopher Kazu

    Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association

    2021  Volume 30, Issue 9, Page(s) 105657

    Abstract: Studying the neuropathologic autopsy findings in subjects with chronic kidney disease (CKD) or chronic renal failure (CRF) is difficult for several reasons: etiology of the CKD may be heterogeneous, affected patients may have one or more major co- ... ...

    Abstract Studying the neuropathologic autopsy findings in subjects with chronic kidney disease (CKD) or chronic renal failure (CRF) is difficult for several reasons: etiology of the CKD may be heterogeneous, affected patients may have one or more major co-morbidities that themselves can cause significant neurologic disease, and agonal events may result in significant findings that were of minimal significance earlier in a patient's life. We studied the constellation of neuropathologic abnormalities in 40 autopsy brains originating from subjects of ages 34-95 years (no children in the study). The most common pathologic change was that of ischemic infarcts (cystic, lacunar and/or microinfarcts), which were seen in over half of subjects. These were associated with both large artery atherosclerosis and arteriolosclerosis (A/S), the latter finding being present in 29/40 subjects. Charcot-Bouchard microaneurysms were present in the brains of three subjects, in one case associated with severe amyloid angiopathy. Microvascular calcinosis (medial sclerosis in the case of arterioles) was seen in the basal ganglia (n=8) and/or endplate region of the hippocampus (n=7) and occasional ischemic infarcts in one brain showed severe calcification. Sequelae of cerebrovascular disease (especially A/S or microvascular disease) are a common neuropathologic substrate for neurologic disability and brain lesions in this complex group of patients. Regulation of calcium metabolism within brain microvessel walls may be worthy of further research in both human brain specimens and animal models.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Animals ; Arteriolosclerosis/etiology ; Arteriolosclerosis/pathology ; Autopsy ; Brain/blood supply ; Cerebral Arteries/pathology ; Cerebral Small Vessel Diseases/etiology ; Cerebral Small Vessel Diseases/pathology ; Cerebrovascular Disorders/etiology ; Cerebrovascular Disorders/pathology ; Female ; Humans ; Male ; Middle Aged ; Renal Insufficiency, Chronic/complications ; Renal Insufficiency, Chronic/diagnosis ; Vascular Calcification/etiology ; Vascular Calcification/pathology
    Language English
    Publishing date 2021-02-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1131675-5
    ISSN 1532-8511 ; 1052-3057
    ISSN (online) 1532-8511
    ISSN 1052-3057
    DOI 10.1016/j.jstrokecerebrovasdis.2021.105657
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Emerging concepts in Alzheimer's disease.

    Vinters, Harry V

    Annual review of pathology

    2015  Volume 10, Page(s) 291–319

    Abstract: Alzheimer's disease/senile dementia of the Alzheimer type (AD/SDAT) is the most common neuropathologic substrate of dementia. It is characterized by synapse loss (predominantly within neocortex) as well as deposition of certain distinctive lesions (the ... ...

    Abstract Alzheimer's disease/senile dementia of the Alzheimer type (AD/SDAT) is the most common neuropathologic substrate of dementia. It is characterized by synapse loss (predominantly within neocortex) as well as deposition of certain distinctive lesions (the result of protein misfolding) throughout the brain. The latter include senile plaques, composed mainly of an amyloid (Aβ) core and a neuritic component; neurofibrillary tangles, composed predominantly of hyperphosphorylated tau; and cerebral amyloid angiopathy, a microangiopathy affecting both cerebral cortical capillaries and arterioles and resulting from Aβ deposition within their walls or (in the case of capillaries) immediately adjacent brain parenchyma. In this article, I discuss the hypothesized role these lesions play in causing cerebral dysfunction, as well as CSF and neuroimaging biomarkers (for dementia) that are especially relevant as immunotherapeutic approaches are being developed to remove Aβ from the brain parenchyma. In addition, I address the role of neuropathology in characterizing the sequelae of new AD/SDAT therapies and helping to validate CSF and neuroimaging biomarkers of disease. Comorbidity of AD/SDAT and various types of cerebrovascular disease is a major theme in dementia research, especially as cognitive impairment develops in the oldest old, who are especially vulnerable to ischemic and hemorrhagic brain lesions.
    MeSH term(s) Alzheimer Disease/diagnosis ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/therapy ; Animals ; Biomarkers/metabolism ; Brain/pathology ; Dementia/pathology ; Humans ; Neurofibrillary Tangles/pathology ; Plaque, Amyloid/pathology
    Chemical Substances Biomarkers
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathol-020712-163927
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Illustrated Neuropathologic Diagnosis of Alzheimer's Disease.

    Doher, Nicholas / Davoudi, Vahid / Magaki, Shino / Townley, Ryan A / Haeri, Mohammad / Vinters, Harry V

    Neurology international

    2023  Volume 15, Issue 3, Page(s) 857–867

    Abstract: As of 2022, the prevalence of Alzheimer's disease (AD) among individuals aged 65 and older is estimated to be 6.2 million in the United States. This figure is predicted to grow to 13.8 million by 2060. An accurate assessment of neuropathologic changes ... ...

    Abstract As of 2022, the prevalence of Alzheimer's disease (AD) among individuals aged 65 and older is estimated to be 6.2 million in the United States. This figure is predicted to grow to 13.8 million by 2060. An accurate assessment of neuropathologic changes represents a critical step in understanding the underlying mechanisms in AD. The current method for assessing postmortem Alzheimer's disease neuropathologic change follows version 11 of the National Alzheimer's Coordinating Center (NACC) coding guidebook. Ambiguity regarding steps in the ABC scoring method can lead to increased time or inaccuracy in staging AD. We present a concise overview of how this postmortem diagnosis is made and relate it to the evolving understanding of antemortem AD biomarkers.
    Language English
    Publishing date 2023-07-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2514727-4
    ISSN 2035-8377 ; 2035-8385
    ISSN (online) 2035-8377
    ISSN 2035-8385
    DOI 10.3390/neurolint15030054
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Severe Polyneuropathy in Hereditary Transthyretin Amyloidosis Caused by H90D Variant.

    Pierce, Joshua / Han, Karam / Vinters, Harry V / Zuckerman, Jonathan E / Halabi, Anasheh

    The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques

    2023  Volume 51, Issue 2, Page(s) 336–338

    MeSH term(s) Humans ; Amyloid Neuropathies, Familial/complications ; Amyloid Neuropathies, Familial/diagnostic imaging ; Amyloid Neuropathies, Familial/genetics ; Polyneuropathies/complications ; Prealbumin/genetics
    Chemical Substances Prealbumin
    Language English
    Publishing date 2023-01-10
    Publishing country England
    Document type Journal Article
    ZDB-ID 197622-9
    ISSN 0317-1671
    ISSN 0317-1671
    DOI 10.1017/cjn.2023.4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Characterization of cerebellar amyloid-β deposits in Alzheimer disease.

    Lopez, Gianluca / Magaki, Shino D / Williams, Christopher Kazu / Paganini-Hill, Annlia / Vinters, Harry V

    Journal of neuropathology and experimental neurology

    2023  Volume 83, Issue 2, Page(s) 72–78

    Abstract: Cerebellar amyloid-β (Aβ) plaques are a component of the diagnostic criteria used in Thal staging and ABC scoring for Alzheimer disease (AD) neuropathologic change. However, Aβ deposits in this anatomic compartment are unique and under-characterized; and ...

    Abstract Cerebellar amyloid-β (Aβ) plaques are a component of the diagnostic criteria used in Thal staging and ABC scoring for Alzheimer disease (AD) neuropathologic change. However, Aβ deposits in this anatomic compartment are unique and under-characterized; and their relationship with other pathological findings are largely undefined. In 73 cases of pure or mixed AD with an A3 score in the ABC criteria, parenchymal (plaques) and vascular (cerebral amyloid angiopathy [CAA]) cerebellar Aβ-42 deposits were characterized with respect to localization, morphology, density, and intensity. Over 85% of cases demonstrated cerebellar Aβ-42 parenchymal staining that correlated with a Braak stage V-VI/B3 score (p < 0.01). Among the 63 with cerebellar Aβ-42 deposits, a diffuse morphology was observed in 75% of cases, compact without a central dense core in 32%, and compact with a central dense core in 16% (all corresponding to plaques evident on hematoxylin and eosin staining). Cases with Purkinje cell (PC) loss showed higher proportions of PC layer Aβ-42 staining than cases without PC loss (88% vs 44%, p = 0.02), suggesting a link between Aβ-42 deposition and PC damage. Among all 73 cases, CAA was observed in the parenchymal vessels of 19% of cases and in leptomeningeal vessels in 44% of cases.
    MeSH term(s) Humans ; Alzheimer Disease/pathology ; Amyloid beta-Peptides/metabolism ; Cerebral Amyloid Angiopathy/pathology ; Cerebellum/pathology ; Plaque, Amyloid/pathology ; Brain/pathology
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2023-12-19
    Publishing country England
    Document type Journal Article
    ZDB-ID 3088-0
    ISSN 1554-6578 ; 0022-3069
    ISSN (online) 1554-6578
    ISSN 0022-3069
    DOI 10.1093/jnen/nlad107
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Hereditary and sporadic cerebral microvascular diseases.

    Vinters, Harry V

    Brain pathology (Zurich, Switzerland)

    2014  Volume 24, Issue 5, Page(s) 494

    MeSH term(s) Brain/blood supply ; Brain/pathology ; Cerebrovascular Disorders/genetics ; Cerebrovascular Disorders/pathology ; Humans ; Microvessels/pathology
    Language English
    Publishing date 2014-01-22
    Publishing country Switzerland
    Document type Introductory Journal Article
    ZDB-ID 1051484-3
    ISSN 1750-3639 ; 1015-6305
    ISSN (online) 1750-3639
    ISSN 1015-6305
    DOI 10.1111/bpa.12176
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Arteriolar neuropathology in cerebral microvascular disease.

    Fang, Chuo / Magaki, Shino D / Kim, Ronald C / Kalaria, Raj N / Vinters, Harry V / Fisher, Mark

    Neuropathology and applied neurobiology

    2022  Volume 49, Issue 1, Page(s) e12875

    Abstract: Cerebral microvascular disease (MVD) is an important cause of vascular cognitive impairment. MVD is heterogeneous in aetiology, ranging from universal ageing to the sporadic (hypertension, sporadic cerebral amyloid angiopathy [CAA] and chronic kidney ... ...

    Abstract Cerebral microvascular disease (MVD) is an important cause of vascular cognitive impairment. MVD is heterogeneous in aetiology, ranging from universal ageing to the sporadic (hypertension, sporadic cerebral amyloid angiopathy [CAA] and chronic kidney disease) and the genetic (e.g., familial CAA, cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy [CADASIL] and cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy [CARASIL]). The brain parenchymal consequences of MVD predominantly consist of lacunar infarcts (lacunes), microinfarcts, white matter disease of ageing and microhaemorrhages. MVD is characterised by substantial arteriolar neuropathology involving ubiquitous vascular smooth muscle cell (SMC) abnormalities. Cerebral MVD is characterised by a wide variety of arteriolar injuries but only a limited number of parenchymal manifestations. We reason that the cerebral arteriole plays a dominant role in the pathogenesis of each type of MVD. Perturbations in signalling and function (i.e., changes in proliferation, apoptosis, phenotypic switch and migration of SMC) are prominent in the pathogenesis of cerebral MVD, making 'cerebral angiomyopathy' an appropriate term to describe the spectrum of pathologic abnormalities. The evidence suggests that the cerebral arteriole acts as both source and mediator of parenchymal injury in MVD.
    MeSH term(s) Humans ; Arterioles/metabolism ; Arterioles/pathology ; Cerebral Infarction/genetics ; Cerebral Infarction/pathology ; CADASIL/pathology ; Brain/pathology ; Cerebral Amyloid Angiopathy/pathology ; Neuromuscular Diseases/pathology
    Language English
    Publishing date 2022-10-19
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80371-6
    ISSN 1365-2990 ; 0305-1846
    ISSN (online) 1365-2990
    ISSN 0305-1846
    DOI 10.1111/nan.12875
    Database MEDical Literature Analysis and Retrieval System OnLINE

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