2,919 results match your criteria Cerebral Amyloid Angiopathy


Clinical and neuropathologic analysis of intracerebral hemorrhage in patients with cerebral amyloid angiopathy.

Clin Neurol Neurosurg 2018 Nov 29;176:110-115. Epub 2018 Nov 29.

Department of Cerebrovascular Surgery, International Medical Center, Saitama Medical University, Hidaka, Saitama, Japan.

Objective: To evaluate the clinical and histopathological features of elderly patients with subcortical intracerebral hemorrhage (ICH), and to analyze the presence of cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD) type pathologic changes using amyloid beta (Aβ) and tau immunohistochemistry.

Patients And Methods: We retrospectively analyzed cases satisfying the Boston criteria for CAA among patients with subcortical hemorrhage who underwent surgical removal by craniotomy at our hospital. Surgical specimens were subjected to hematoxylin and eosin (HE) staining as well as immunostaining. Read More

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http://dx.doi.org/10.1016/j.clineuro.2018.11.020DOI Listing
November 2018

Transmission of amyloid-β protein pathology from cadaveric pituitary growth hormone.

Nature 2018 Dec 13. Epub 2018 Dec 13.

MRC Prion Unit at UCL, UCL Institute of Prion Diseases, London, UK.

We previously reported the presence of amyloid-β protein (Aβ) deposits in individuals with Creutzfeldt-Jakob disease (CJD) who had been treated during childhood with human cadaveric pituitary-derived growth hormone (c-hGH) contaminated with prions. The marked deposition of parenchymal and vascular Aβ in these relatively young individuals with treatment-induced (iatrogenic) CJD (iCJD), in contrast to other prion-disease patients and population controls, allied with the ability of Alzheimer's disease brain homogenates to seed Aβ deposition in laboratory animals, led us to argue that the implicated c-hGH batches might have been contaminated with Aβ seeds as well as with prions. However, this was necessarily an association, and not an experimental, study in humans and causality could not be concluded. Read More

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http://www.nature.com/articles/s41586-018-0790-y
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http://dx.doi.org/10.1038/s41586-018-0790-yDOI Listing
December 2018
12 Reads

Subarachnoid extension of lobar hemorrhage on acute/subacute MRI is associated with cerebral amyloid angiopathy criteria.

Acta Neurol Belg 2018 Dec 11. Epub 2018 Dec 11.

Department of Neurology, CHU Nîmes, Hôpital Caremeau, Nîmes University Hospital, 4, Rue du Pr Debré, 30029, Nîmes Cedex 4, France.

Subarachnoid hemorrhage extension (SAHE) in the acute phase of cerebral amyloid angiopathy (CAA)-related lobar hemorrhage (LH) assessed by CT is very frequent. Recently, SAHE, together with finger-like projections on CT and ApoE4, has been used in a prediction model for histopathologically proven CAA showing excellent discrimination. Our aim was to analyze SAHE on MRI in the acute and subacute phase of LH in patients with and without associated hemorrhagic features supportive of CAA (i. Read More

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http://dx.doi.org/10.1007/s13760-018-01060-9DOI Listing
December 2018
1 Read

Successful mechanical thrombectomy in stroke with thrombolysis-associated intracerebral hemorrhage-a case report.

J Stroke Cerebrovasc Dis 2018 Oct 24. Epub 2018 Oct 24.

Department of Neurology, University Hospital Bonn, Bonn, Germany; German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany. Electronic address:

Background: Intravenous thrombolysis and mechanical thrombectomy are the standard of care for patients with acute ischemic stroke with large vessel occlusion. Intracerebral hemorrhage is a main complication of intravenous thrombolysis, however, no data are available on the efficacy and safety of mechanical thrombectomy in patients with thrombolysis-associated intracerebral hemorrhage. This constellation is expected to become more frequent as increasing numbers of patients are treated under the drip-and-ship paradigm. Read More

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http://dx.doi.org/10.1016/j.jstrokecerebrovasdis.2018.09.045DOI Listing
October 2018

Primary central nervous system vasculitis mimicking brain tumor: Comprehensive analysis of 13 cases from a single institutional cohort of 191 cases.

J Autoimmun 2018 Oct 24. Epub 2018 Oct 24.

Division of Rheumatology, Mayo Clinic, Rochester, MN, USA.

Objective: To describe the clinical, laboratory, and imaging features and course of patients with primary central nervous system vasculitis (PCNSV) presenting with an intracranial tumor-like mass (TLM).

Methods: We retrospectively studied a cohort of 191 consecutive patients with PCNSV seen at the Mayo Clinic, Rochester, MN over a 35-year period (1982-2017). 13/191 patients presented with a TLM. Read More

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http://dx.doi.org/10.1016/j.jaut.2018.10.001DOI Listing
October 2018

Mouse models of Alzheimer's disease cause rarefaction of pial collaterals and increased severity of ischemic stroke.

Angiogenesis 2018 Dec 5. Epub 2018 Dec 5.

Department of Cell Biology and Physiology, University of North Carolina at Chapel Hill, 6309 MBRB, Chapel Hill, NC, 27599-7545, USA.

Vascular dysfunction contributes to the progression and severity of Alzheimer's disease (AD). Patients with AD also sustain larger infarctions after ischemic stroke; however, the responsible mechanisms are unknown. Pial collaterals are the primary source of protection in stroke. Read More

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http://dx.doi.org/10.1007/s10456-018-9655-0DOI Listing
December 2018
1 Read
4.876 Impact Factor

The Role of NADPH Oxidases and Oxidative Stress in Neurodegenerative Disorders.

Int J Mol Sci 2018 Nov 30;19(12). Epub 2018 Nov 30.

Institute of Biomedical and Clinical Sciences (IBCS), College of Medicine and Health (CMH), St. Luke's Campus, University of Exeter, Exeter EX4 4QL, UK.

For a number of years, nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) was synonymous with NOX2/gp91 and was considered to be a peculiarity of professional phagocytic cells. Over the last decade, several more homologs have been identified and based on current research, the NOX family consists of NOX1, NOX2, NOX3, NOX4, NOX5, DUOX1 and DUOX2 enzymes. NOXs are electron transporting membrane proteins that are responsible for reactive oxygen species (ROS) generation-primarily superoxide anion (O₂), although hydrogen peroxide (H₂O₂) can also be generated. Read More

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http://www.mdpi.com/1422-0067/19/12/3824
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http://dx.doi.org/10.3390/ijms19123824DOI Listing
November 2018
5 Reads

Aging and cerebrovascular lesions in pure and in mixed neurodegenerative and vascular dementia brains: a neuropathological study.

Folia Neuropathol 2018 ;56(2):81-87

Introduction: The prevalence of dementia is increasing in our aging population. Because of the complexity of disease pathology, dementia classifications remain controversial. The present post-mortem study investigates whether there are age differences between dementia brains with a single pure neurodegenerative or cerebrovascular disease and those with mixed pathological features. Read More

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http://dx.doi.org/10.5114/fn.2018.76610DOI Listing
January 2018
1 Read

The cAMP/PKA Pathway Inhibits Beta-amyloid Peptide Release from Human Platelets.

Neuroscience 2018 Nov 26;397:159-171. Epub 2018 Nov 26.

Thrombosis Reasearch Center, Department of Clinical Biochemistry and Immunohematology, Faculty of Health Sciences, Chile; Interdisciplinary Excellence Research Program on Healthy Aging (PIEI-ES), Universidad de Talca, Talca 3460000, Chile; Centro de Estudios en Alimentos Procesados (CEAP), CONICYT-Regional, Gore Maule, R09I2001 Talca, Chile. Electronic address:

The main component of Alzheimer's disease (AD) is the amyloid-beta peptide (Aβ), the brain of these patients is characterized by deposits in the parenchyma and cerebral blood vessels known as cerebral amyloid angiopathy (CAA). On the other hand, the platelets are the major source of the Aβ peptide in circulation and once secreted can activate the platelets and endothelial cells producing the secretion of several inflammatory mediators that finally end up unchaining the CAA and later AD. In the present study we demonstrate that cAMP/PKA pathway plays key roles in the regulation of calpain activation and secretion of Aβ in human platelets. Read More

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http://dx.doi.org/10.1016/j.neuroscience.2018.11.025DOI Listing
November 2018
3 Reads

Extravascular fibrinogen in the white matter of Alzheimer's disease and normal aged brains: implications for fibrinogen as a biomarker for Alzheimer's disease.

Brain Pathol 2018 Nov 28. Epub 2018 Nov 28.

Institute of Neuroscience, Newcastle University, Newcastle Upon Tyne, UK.

The blood-brain barrier (BBB) regulates cerebrovascular permeability and leakage of blood-derived fibrinogen has been associated with cerebral arteriolosclerosis small vessel disease (SVD) and subsequent white matter lesions (WML). Furthermore, BBB-dysfunction is associated with the pathogenesis of Alzheimer's disease (AD) with the presence of CSF plasma proteins suggested to be a potential biomarker of AD. We aimed to determine if extravascular fibrinogen in the white matter was associated with the development of AD hallmark pathologies, i. Read More

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http://dx.doi.org/10.1111/bpa.12685DOI Listing
November 2018

Blood-Brain Barrier Dysfunction in Small Vessel Disease Related Intracerebral Hemorrhage.

Front Neurol 2018 12;9:926. Epub 2018 Nov 12.

Department of Neurology, Center for Neuroscience, Donders Institute for Brain Cognition & Behaviour, Radboud University Medical Center, Nijmegen, Netherlands.

Hypertensive vasculopathy and cerebral amyloid angiopathy are the two most common forms of cerebral small vessel disease. Both forms are associated with the development of primary intracerebral hemorrhage, but the pathophysiological mechanisms underlying spontaneous vessel rupture remain unknown. This work constitutes a systematic review on blood-brain barrier dysfunction in the etiology of spontaneous intracerebral hemorrhage due to cerebral small vessel disease. Read More

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http://dx.doi.org/10.3389/fneur.2018.00926DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6240684PMC
November 2018

Multiple infarcts and hemorrhages in the central nervous system of a dog with cerebral amyloid angiopathy: a case report.

BMC Vet Res 2018 Nov 27;14(1):370. Epub 2018 Nov 27.

Departament of Pathology, Faculdade de Medicina Veterinária e Zootecnia, Universidade de São Paulo, Av. Prof Dr. Orlando Marques de Paiva, 87, São Paulo, 05508-270, Brazil.

Background: β-amyloid (Aβ) can accumulate in the brain of aged dogs, and within vessels walls, the disease is called cerebral amyloid angiopathy (CAA). In humans, Alzheimer's disease and CAA are strongly correlated with cerebrovascular disease. However, in dogs, this association has not been extensively studied yet. Read More

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http://dx.doi.org/10.1186/s12917-018-1700-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6258392PMC
November 2018
1 Read

Angiopoietin like-4 as a novel vascular mediator in capillary cerebral amyloid angiopathy.

Brain 2018 Dec;141(12):3377-3388

Amsterdam UMC, Vrije Universiteit Amsterdam, Department of Molecular Cell Biology and Immunology, Amsterdam Neuroscience, The Netherlands.

Increasing evidence suggests that vascular dysfunction in the brain is associated with early stages of Alzheimer's disease. Amyloid-β deposition in the microvasculature of the brain, a process referred to as capillary cerebral amyloid angiopathy (capillary CAA), propagates vascular remodelling, which results in impaired function of the blood-brain barrier, reduced cerebral perfusion and increased hypoxia. While improving vascular function may be an attractive new way to fight capillary CAA, the underlying factors that mediate vascular alterations in Alzheimer's disease and capillary CAA pathogenesis remain largely unknown. Read More

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http://dx.doi.org/10.1093/brain/awy274DOI Listing
December 2018
5 Reads

Progressive Supranuclear Palsy-like Syndrome from Possible Cerebral Amyloid Angiopathy.

Can J Neurol Sci 2018 Nov 20:1-5. Epub 2018 Nov 20.

Division of Neurology, Department of Medicine,University of Alberta,Edmonton, Alberta,Canada.

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http://dx.doi.org/10.1017/cjn.2018.367DOI Listing
November 2018
1 Read

Teaching Video NeuroImages: Cerebral amyloid angiopathy-related transient focal neurologic episodes: A video-EEG report.

Neurology 2018 Nov;91(21):e2033-e2034

From the Departments of Neurology (A.V., P.G., N.R., L.C., M.D., L.V., J.M.O., J.F.A., J.C.) and Neuroradiology (F.B.), Hôpital Pierre-Paul Riquet, Centre Hospitalier Universitaire de Toulouse; Toulouse NeuroImaging Center (A.V., N.R., L.C., J.M.O., J.F.A., F.B.), Université de Toulouse, INSERM U1214, UPS; CerCo (L.V., J.C.), CNRS, UMR5549, Toulouse Mind and Brain Institute; and Centre de Recherche Cerveau et Cognition (L.V., J.C.), Université de Toulouse, UPS, France.

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http://dx.doi.org/10.1212/WNL.0000000000006555DOI Listing
November 2018
2 Reads

Microbleeds and Cerebral Amyloid Angiopathy in the Brains of People with Down Syndrome with Alzheimer's Disease.

J Alzheimers Dis 2018 Nov 15. Epub 2018 Nov 15.

Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA.

Cerebrovascular pathology is a significant mediator in Alzheimer's disease (AD) in the general population. In people with Down syndrome (DS), the contribution of vascular pathology to dementia may play a similar role in age of onset and/or the rate of progression of AD. In the current study, we explored the extent of microbleeds (MBs) and the link between cerebral amyloid angiopathy (CAA) and MBs in the frontal cortex (FCTX) and occipital cortex (OCTX) in an autopsy series from individuals with DS (<40 years), DS with AD pathology (DSAD), sporadic AD, and control cases (2-83 years). Read More

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http://dx.doi.org/10.3233/JAD-180589DOI Listing
November 2018
3 Reads

A Novel Transgenic Rat Model of Robust Cerebral Microvascular Amyloid with Prominent Vasculopathy.

Am J Pathol 2018 Dec 13;188(12):2877-2889. Epub 2018 Nov 13.

George and Anne Ryan Institute for Neuroscience, University of Rhode Island, Kingston, Rhode Island; Department of Biomedical and Pharmaceutical Sciences, University of Rhode Island, Kingston, Rhode Island. Electronic address:

Accumulation of fibrillar amyloid β protein in blood vessels of the brain, a condition known as cerebral amyloid angiopathy (CAA), is a common pathology of elderly individuals, a prominent comorbidity of Alzheimer disease, and a driver of vascular cognitive impairment and dementia. Although several transgenic mouse strains have been generated that develop varying levels of CAA, consistent models of associated cerebral microhemorrhage and vasculopathy observed clinically have been lacking. Reliable preclinical animal models of CAA and microhemorrhage are needed to investigate the molecular pathogenesis of this condition. Read More

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https://linkinghub.elsevier.com/retrieve/pii/S00029440183049
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http://dx.doi.org/10.1016/j.ajpath.2018.07.030DOI Listing
December 2018
4 Reads
4.591 Impact Factor

[Risk factors for hypertensive and cerebral amyloid angiopathy associated intracerebral hemorrhage: a retrospective comparison].

Fortschr Neurol Psychiatr 2018 Nov 12. Epub 2018 Nov 12.

Klinik für Neurologie, HELIOS Kliniken Schwerin, Schwerin, Deutschland.

Introduction: The aim of this study was to compare possible risk factors for the most common forms of spontaneous intracerebral hemorrhage (ICH), namely hypertensive and cerebral amyloid angiopathy (CAA) associated ICH.

Methods: Retrospectively, different parameters and factors were compared in patients with hypertensive ICH (n = 141) and patients with a CAAassociated ICH (n = 95). These included age, INR value and blood pressure at admission, cardiovascular risk factors as well as pre-medication. Read More

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http://www.thieme-connect.de/DOI/DOI?10.1055/a-0732-5523
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http://dx.doi.org/10.1055/a-0732-5523DOI Listing
November 2018
4 Reads

The Prevalence of Cerebral Microbleeds in Non-Demented Parkinson's Disease Patients.

J Korean Med Sci 2018 Nov 19;33(46):e289. Epub 2018 Oct 19.

Department of Neurology, Seoul National University Bundang Hospital, Seoul National University Hospital, Seoul National University College of Medicine, Seongnam, Korea.

Background: Cerebral microbleeds (CMBs) are associated with cerebrovascular risk factors and cognitive dysfunction among patients with Parkinson's disease (PD). However, whether CMBs themselves are associated with PD is to be elucidated.

Methods: We analyzed the presence of CMBs using 3-Tesla brain magnetic resonance imaging in non-demented patients with PD and in age-, sex-, and hypertension-matched control subjects. Read More

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http://dx.doi.org/10.3346/jkms.2018.33.e289DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6221857PMC
November 2018
3 Reads

Amyloid precursor protein-fragments-containing inclusions in cardiomyocytes with basophilic degeneration and its association with cerebral amyloid angiopathy and myocardial fibrosis.

Sci Rep 2018 Nov 9;8(1):16594. Epub 2018 Nov 9.

Institute of Pathology, Ulm University, Ulm, Germany.

Cardiomyopathies with intracellular inclusions are a distinct subset of cardiomyopathies whereas basophilic degeneration (BD) of the heart describes inclusions in cardiomyocytes of the aging heart, which have not yet been related to a specific disease condition or to a distinct type of protein inclusion. To address the question whether BD represents a specific pathological feature and whether it is linked to a distinct disease condition we studied 62 autopsy cases. BD inclusions exhibited an immunohistochemical staining pattern related to glycosylated, δ- or η-secretase-derived N-terminal cleavage products of the amyloid precursor protein (sAPPδ/η) or shorter fragments of sAPPη. Read More

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http://www.nature.com/articles/s41598-018-34808-7
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http://dx.doi.org/10.1038/s41598-018-34808-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6226444PMC
November 2018
5 Reads
5.080 Impact Factor

AlF-NODA Benzothiazole Derivatives as Imaging Agents for Cerebrovascular Amyloid in Cerebral Amyloid Angiopathy.

ACS Omega 2018 Oct 12;3(10):13089-13096. Epub 2018 Oct 12.

Department of Nuclear Medicine, Chinese PLA General Hospital, Beijing 100853, P. R. China.

In this study, we synthesized four novel AlF-labeled 2-phenylbenzothiazole derivatives conjugated to 1,4,7-triazacyclononane-1,4-diacetic acid via alkyl linkers and evaluated them as imaging agent targets to amyloid-β (Aβ) plaques deposited in the blood vessels of cerebral amyloid angiopathy (CAA) brain. The four ligands exhibited moderate-to-high binding ability to Aβ aggregates, of which complex possessing the most potent affinity ( = 11.3 nM) was selected for further biological evaluations. Read More

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http://pubs.acs.org/doi/10.1021/acsomega.8b01120
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http://dx.doi.org/10.1021/acsomega.8b01120DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6217595PMC
October 2018
5 Reads

β-amyloid wall deposit of temporal artery in subjects with spontaneous intracerebral haemorrhage.

Oncotarget 2018 Oct 5;9(78):34699-34707. Epub 2018 Oct 5.

Internal Medicine and Stroke Care Ward, Dipartimento Biomedico di Medicina Interna e Specialistica, University of Palermo, Palermo, Italy.

Background: Cerebral Amyloid Angiopathy has been indicated as an important cause of spontaneous non-hypertensive intracerebral haemorrhage (ICH).

Aims: to analyze the presence of β-amyloid deposit in the temporal artery of consecutive patients with ICH in comparison to control subjects and its relation to APO-E haplotype frequency.

Methods: We enrolled consecutive patients admitted to Neurosurgery Ward of University Hospital "P. Read More

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http://www.oncotarget.com/fulltext/26165
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http://dx.doi.org/10.18632/oncotarget.26165DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6205179PMC
October 2018
3 Reads

Coagulation factor XIIIa crosslinks amyloid b into dimers and oligomers and to blood proteins.

J Biol Chem 2018 Nov 8. Epub 2018 Nov 8.

Michael Smith Laboratories, University of British Columbia, Canada.

In cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), the amyloid β(Aβ) peptide deposits along the vascular lumen, leading to degeneration and dysfunction of surrounding tissues. Activated coagulation factor XIIIa (FXIIIa) covalently crosslinks proteins in blood and vasculature, such as in blood clots and on the extracellular matrix. Although FXIIIa co-localizes with Aβ in CAA, the ability of FXIIIa to crosslink Aβ has not been demonstrated. Read More

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http://dx.doi.org/10.1074/jbc.RA118.005352DOI Listing
November 2018
4 Reads

Azelnidipine Attenuates the Oxidative and NFκB Pathways in Amyloid-β-Stimulated Cerebral Endothelial Cells.

ACS Chem Neurosci 2018 Nov 8. Epub 2018 Nov 8.

Richard and Loan Hill Department of Bioengineering , University of Illinois at Chicago , 851 South Morgan Street, MC 063 , Chicago , Illinois 60607 , United States.

Cerebral amyloid angiopathy (CAA), a condition depicting cerebrovascular accumulation of amyloid β-peptide (Aβ), is a common pathological manifestation in Alzheimer's disease (AD). In this study, we investigated the effects of Azelnidipine (ALP), a dihydropyridine calcium channel blocker known for its treatment of hypertension, on oligomeric Aβ (oAβ)-induced calcium influx and its downstream pathway in immortalized mouse cerebral endothelial cells (bEND3). We found that ALP attenuated oAβ-induced calcium influx, superoxide anion production, and phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and calcium-dependent cytosolic phospholipase A (cPLA). Read More

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http://pubs.acs.org/doi/10.1021/acschemneuro.8b00368
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http://dx.doi.org/10.1021/acschemneuro.8b00368DOI Listing
November 2018
5 Reads

Distinct amyloid distribution patterns in amyloid positive subcortical vascular cognitive impairment.

Sci Rep 2018 Nov 1;8(1):16178. Epub 2018 Nov 1.

Departments of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea.

Amyloid-β (Aβ) and cerebral small vessel disease (CSVD) commonly coexist. They can occur independently by chance, or may interact with each other. We aimed to determine whether the distribution of Aβ in subcortical vascular cognitive impairments (SVCI) patients can be classified by the underlying pathobiologies. Read More

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http://dx.doi.org/10.1038/s41598-018-34032-3DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6212495PMC
November 2018
5 Reads

Becoming a Caregiver - Lessons from My Dad.

N Engl J Med 2018 Nov;379(18):1696-1697

From the Massachusetts General Hospital Chelsea Health Center, Chelsea.

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http://dx.doi.org/10.1056/NEJMp1808685DOI Listing
November 2018

Cerebral Cortical Microinfarcts on Magnetic Resonance Imaging and Their Association With Cognition in Cerebral Amyloid Angiopathy.

Stroke 2018 Oct;49(10):2330-2336

From the Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston (L.X., S.J.v.V., N.B., A.C., M.P., A.-K.G., P.F., G.R., K.S., E.M.G., A.B., S.M.G., A.V.).

Background and Purpose- We aimed to explore the association between presence of cerebral cortical microinfarcts (CMIs) on magnetic resonance imaging and other small-vessel disease neuroimaging biomarkers in cerebral amyloid angiopathy (CAA) and to analyze the role of CMIs on individual cognitive domains and dementia conversion. Methods- Participants were recruited from an ongoing longitudinal research cohort of eligible CAA patients between March 2006 and October 2016. A total of 102 cases were included in the analysis that assessed the relationship of cortical CMIs to CAA neuroimaging markers. Read More

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https://www.ahajournals.org/doi/10.1161/STROKEAHA.118.022280
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http://dx.doi.org/10.1161/STROKEAHA.118.022280DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6209124PMC
October 2018
4 Reads

Cerebral Amyloid Angiopathy With Vascular Iron Accumulation and Calcification.

Stroke 2018 Sep;49(9):2081-2087

From the Department of Radiology (M.B., L.G.M., L.M.v.d.G., M.A.v.B., S.v.R., L.v.d.W.).

Background and Purpose- Previous studies of symptomatic and asymptomatic hereditary cerebral amyloid angiopathy (CAA) patients offered the possibility to study the radiological manifestations of CAA in the early stages of the disease. Recently, a striped cortex, observable as hypointense lines perpendicular to the pial surface on T-weighted 7T magnetic resonance imaging (MRI), was detected in 40% of the symptomatic hereditary CAA patients. However, the origin of these MRI contrast changes is unknown. Read More

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http://dx.doi.org/10.1161/STROKEAHA.118.021872DOI Listing
September 2018
4 Reads

Platelets isolated from an Alzheimer mouse damage healthy cortical vessels and cause inflammation in an organotypic ex vivo brain slice model.

Sci Rep 2018 Oct 19;8(1):15483. Epub 2018 Oct 19.

Laboratory of Psychiatry and Exp. Alzheimer's Research, Department of Psychiatry I, Medical University of Innsbruck, Innsbruck, Austria.

Platelets are anuclear blood cells and play a major role in hemostasis and thrombosis. Platelets express amyloid-precursor protein (APP), release beta-amyloid (Aβ) and are stimulated (pre-activated) in Alzheimer's disease (AD). We hypothesize that such stimulated platelets severely damage brain vessels which subsequently leads to cerebrovascular damage in AD. Read More

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http://dx.doi.org/10.1038/s41598-018-33768-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6195547PMC
October 2018

Elimination of substances from the brain parenchyma: efflux via perivascular pathways and via the blood-brain barrier.

Fluids Barriers CNS 2018 Oct 19;15(1):30. Epub 2018 Oct 19.

Department of Pharmacology, University of Cambridge, Cambridge, CB2 1PD, UK.

This review considers efflux of substances from brain parenchyma quantified as values of clearances (CL, stated in µL g min). Total clearance of a substance is the sum of clearance values for all available routes including perivascular pathways and the blood-brain barrier. Perivascular efflux contributes to the clearance of all water-soluble substances. Read More

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http://dx.doi.org/10.1186/s12987-018-0113-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6194691PMC
October 2018

Neuropolypathology as a result of severe traumatic brain injury?

Clin Neuropathol 2018 Oct 19. Epub 2018 Oct 19.

A history of brain trauma has long been acknowledged as increasing an individual's risk of developing dementia in later life. The underlying mechanisms that belie this pre-disposition are, however, very poorly understood. Here, we report a clinical-neuropathological correlation of a man who presented at the age of 66 with a progressive complex atypical dementia with early and prominent neurobehavioral symptoms. Read More

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http://dx.doi.org/10.5414/NP301131DOI Listing
October 2018
1 Read

Sex differences in Alzheimer's disease and common neuropathologies of aging.

Acta Neuropathol 2018 Dec 17;136(6):887-900. Epub 2018 Oct 17.

Rush Alzheimer's Disease Center, Rush University Medical Center, 1750 W Harrison, Suite 1000, Chicago, IL, USA.

Alzheimer's dementia is significantly more common in women than in men. However, few pathological studies have addressed sex difference in Alzheimer's disease (AD) and other brain pathologies. We leveraged postmortem data from 1453 persons who participated in one of two longitudinal community-based studies of older adults, the Religious Orders Study and the Rush Memory and Aging Project. Read More

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http://dx.doi.org/10.1007/s00401-018-1920-1DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6279593PMC
December 2018
7 Reads

Cationic carrier peptide enhances cerebrovascular targeting of nanoparticles in Alzheimer's disease brain.

Nanomedicine 2018 Oct 6. Epub 2018 Oct 6.

Department of Pharmaceutics and Brain Barriers Research Center, College of Pharmacy, University of Minnesota, Minneapolis, MN, USA; Molecular Neurobiology Laboratory, Departments of Neurology, Neuroscience and Biochemistry/Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA. Electronic address:

Accumulation of amyloid beta (Aβ) peptides in the cerebral vasculature, referred to as cerebral amyloid angiopathy (CAA), is widely observed in Alzheimer's disease (AD) brain and was shown to accelerate cognitive decline. There is no effective method for detecting cerebrovascular amyloid (CVA) and treat CAA. The targeted nanoparticles developed in this study effectively migrated from the blood flow to the vascular endothelium as determined by using quartz crystal microbalance with dissipation monitoring (QCM-D) technology. Read More

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http://dx.doi.org/10.1016/j.nano.2018.09.010DOI Listing
October 2018
5 Reads

Increased cerebral microbleeds and cortical superficial siderosis in pediatric patients with Down syndrome.

Eur J Paediatr Neurol 2018 Sep 12. Epub 2018 Sep 12.

Department of Radiology, University Hospital, LMU Munich, Marchioninistr. 15, 81377, Munich, Germany; Department of Radiology, The Hospital for Sick Children, 555 University Ave, Toronto, ON M5G1X8, Canada.

Background: Patients with Down syndrome carry a third copy of the amyloid precursor protein gene, which is localized on chromosome 21. Consequently, these patients are prone to develop early-onset Alzheimer disease and cerebral amyloid angiopathy. Post-mortem studies suggest increased amyloid deposition to be already detectable in children with Down syndrome. Read More

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http://dx.doi.org/10.1016/j.ejpn.2018.09.004DOI Listing
September 2018
1 Read

Serum Markers of Blood-Brain Barrier Remodeling and Fibrosis as Predictors of Etiology and Clinicoradiologic Outcome in Intracerebral Hemorrhage.

Front Neurol 2018 7;9:746. Epub 2018 Sep 7.

Neuroscience Department, Kaiser Permanente, Redwood City, CA, United States.

Intracerebral hemorrhage (ICH) is a stroke subtype associated with high disability and mortality. There is a clinical need for blood-based biomarkers that can aid in diagnosis, risk stratification, and prognostication. Given their role in the pathophysiology of ICH, we hypothesized markers of blood-brain barrier disruption and fibrosis would associate with neurologic deterioration and/or long-term functional outcomes. Read More

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https://www.frontiersin.org/article/10.3389/fneur.2018.00746
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http://dx.doi.org/10.3389/fneur.2018.00746DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6143812PMC
September 2018
9 Reads

Cerebral Small Vessel Disease.

Cell Transplant 2018 Dec 25;27(12):1711-1722. Epub 2018 Sep 25.

3 Department of Physiology and Pharmacology, Loma Linda University School of Medicine, Loma Linda, CA, USA.

Cerebral small vessel disease (CSVD) is composed of several diseases affecting the small arteries, arterioles, venules, and capillaries of the brain, and refers to several pathological processes and etiologies. Neuroimaging features of CSVD include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. The main clinical manifestations of CSVD include stroke, cognitive decline, dementia, psychiatric disorders, abnormal gait, and urinary incontinence. Read More

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http://dx.doi.org/10.1177/0963689718795148DOI Listing
December 2018
8 Reads
3.570 Impact Factor

Journal Club: Florbetapir imaging in cerebral amyloid angiopathy-related hemorrhages.

Neurology 2018 Sep;91(12):574-577

From the Hemorrhagic Stroke Research Program, Department of Neurology, Massachusetts General Hospital Stroke Research Center, Harvard Medical School, Boston.

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http://dx.doi.org/10.1212/WNL.0000000000006195DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6161557PMC
September 2018
1 Read

The Clinical Dilemma of Anticoagulation Use in Patients with Cerebral Amyloid Angiopathy and Atrial Fibrillation.

Curr Cardiol Rep 2018 Sep 12;20(11):106. Epub 2018 Sep 12.

From the Department of Neurology (RJC, JFM), Mayo Clinic in Florida, 4500 San Pablo Road, Jacksonville, FL, 32256, USA.

Purpose Of Review: This review highlights current management of patients with concomitant cerebral amyloid angiopathy (CAA) and atrial fibrillation (AF). We review quantifying risk of ischemic and hemorrhagic stroke as well as treatments to minimize future risk.

Recent Findings: Ischemic stroke risk in AF can be quantified by CHADS-VASc and assessing left atrial echocardiographic characteristics. Read More

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http://dx.doi.org/10.1007/s11886-018-1052-1DOI Listing
September 2018
2 Reads

Blood-brain barrier integrity in a mouse model of Alzheimer's disease with or without acute 3D6 immunotherapy.

Neuropharmacology 2018 Dec 7;143:1-9. Epub 2018 Sep 7.

Department of Public Health and Caring Sciences, Molecular Geriatrics, Dag Hammarskjölds väg 20, 751 85, Uppsala, Sweden. Electronic address:

The blood-brain barrier (BBB) is suggested to be compromised in Alzheimer's disease (AD). The concomitant presence of vascular amyloid beta (Aβ) pathology, so called cerebral amyloid angiopathy (CAA), also predisposes impairment of vessel integrity. Additionally, immunotherapy against Aβ may lead to further damage of the BBB. Read More

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http://dx.doi.org/10.1016/j.neuropharm.2018.09.001DOI Listing
December 2018
2 Reads

Fibronectin induces the perivascular deposition of cerebrospinal fluid-derived amyloid-β in aging and after stroke.

Neurobiol Aging 2018 Dec 9;72:1-13. Epub 2018 Aug 9.

Department of Neurology, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA. Electronic address:

Cerebral amyloid angiopathy occurs after stroke, but the mechanism underlying the initial amyloid-β deposition is not fully understood. This study investigates whether overexpression of fibronectin and its receptor, integrin-α5, induces the perivascular deposition of cerebrospinal fluid-derived amyloid-β after stroke in young and aged animals. We found that stroke impaired the bulk flow of cerebrospinal fluid into the brain parenchyma and further showed that perivascular amyloid-β deposition was enhanced in aged animals with stroke, which colocalized with integrin-α5 in the basement membrane. Read More

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http://dx.doi.org/10.1016/j.neurobiolaging.2018.07.019DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6219378PMC
December 2018

Assessment of pathological features in Alzheimer's disease brain tissue with a large field-of-view visible-light optical coherence microscope.

Neurophotonics 2018 Jul 24;5(3):035002. Epub 2018 Jul 24.

Medical University of Vienna, Center for Medical Physics and Biomedical Engineering, Vienna, Austria.

We implemented a wide field-of-view visible-light optical coherence microscope (OCM) for investigating brain tissue of patients diagnosed with Alzheimer's disease (AD) and of a mouse model of AD. A submicrometer axial resolution in tissue was achieved using a broad visible light spectrum. The use of various objective lenses enabled reaching micrometer transversal resolution and the acquisition of images of microscopic brain features, such as cell structures, vessels, and white matter tracts. Read More

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http://dx.doi.org/10.1117/1.NPh.5.3.035002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057230PMC
July 2018
3 Reads

Hemorrhagic and non-hemorrhagic causes of signal loss on susceptibility-weighted imaging.

Emerg Radiol 2018 Dec 22;25(6):691-701. Epub 2018 Aug 22.

Department of Imaging Sciences, University of Rochester Medical Center, 601 Elmwood Avenue, PO Box 648, Rochester, NY, 14642, USA.

Susceptibility-weighted imaging (SWI) plays a key role in an emergency setting. SWI takes the intrinsic properties of materials being scanned and creates a visual representation of their effects on the magnetic field, thereby differentiating a number of pathologies. Magnetic resonance imaging (MRI) is now more often used, especially when computed tomography (CT) is inconclusive or even negative. Read More

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http://link.springer.com/10.1007/s10140-018-1634-7
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http://dx.doi.org/10.1007/s10140-018-1634-7DOI Listing
December 2018
10 Reads

Domain-specific characterisation of early cognitive impairment following spontaneous intracerebral haemorrhage.

J Neurol Sci 2018 Aug 21;391:25-30. Epub 2018 May 21.

Stroke Research Centre, Department of Brain Repair and Rehabilitation, UCL Institute of Neurology and the National Hospital for Neurology and Neurosurgery, London, UK. Electronic address:

Cognitive deficits after spontaneous intracerebral haemorrhage (ICH) are common and result in functional impairment, but few studies have examined deficits across cognitive domains in the subacute phase. This study aims to describe the cognitive profile following acute ICH and explore how cerebral amyloid angiopathy (CAA) may impact performance. We retrospectively reviewed 187 consecutive patients with ICH (mean age 58. Read More

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http://dx.doi.org/10.1016/j.jns.2018.05.015DOI Listing
August 2018
2 Reads

The presence of cerebral microbleeds is associated with cognitive impairment in Parkinson's disease.

J Neurol Sci 2018 Oct 8;393:39-44. Epub 2018 Aug 8.

Department of Neurology, Juntendo University, 2-1-1, Hongo, Bunkyo ward, Tokyo, 113-0033, Japan. Electronic address:

Background: Cerebral microbleeds (CMBs) are often observed in Parkinson's disease (PD); however, their association with cognitive decline has been unclear. We performed a retrospective analysis of 124 cases of clinically diagnosed PD to determine the association between the presence of CMBs and cognitive decline.

Results: Of the 124 participants, 21 (16. Read More

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http://dx.doi.org/10.1016/j.jns.2018.08.009DOI Listing
October 2018
13 Reads

[ROLA I WARTOŚĆ ROKOWNICZA MIKROKRWAWIEŃ MÓZGOWYCH W SCHORZENIACH NEUROLOGICZNYCH THE ROLE AND PROGNOSTIC VALUE OF CEREBRAL MICROBLEEDS IN NEUROLOGICAL DISORDERS 907].

Wiad Lek 2018;71(4):907-912

Katedra i Klinika Neurologii Uniwersytetu Medycznego w Lublinie, Lublin, Polska.

Cerebral microbleeds (CMB) are small foci of low signal which are detected in neuroimaging. They correspond to hemosiderin and other blood breakdown products from brain vessels whose structure was affected by pathological processes. Their pathogenesis is closely related to angiopathy associated with hypertension and cerebral amyloid angiopathy. Read More

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October 2018
7 Reads

Alzheimer's disease neuropathology may not predict functional impairment in HIV: a report of two individuals.

J Neurovirol 2018 Oct 9;24(5):629-637. Epub 2018 Aug 9.

Department of Neuroscience and Pathology, The Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.

With aging of HIV populations, there is concern that Alzheimer's disease (AD) may become prevalent and difficult to distinguish from HIV-associated neurocognitive disorders. To date, there are no reports documenting histologically verified Alzheimer's neuropathology in individuals with HIV and dementia. Herein, we report two antiretroviral-treated, virally suppressed, HIV-infected individuals autopsied by the Manhattan HIV Brain Bank. Read More

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http://dx.doi.org/10.1007/s13365-018-0663-zDOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6202220PMC
October 2018
12 Reads

Different curcumin forms selectively bind fibrillar amyloid beta in post mortem Alzheimer's disease brains: Implications for in-vivo diagnostics.

Acta Neuropathol Commun 2018 Aug 9;6(1):75. Epub 2018 Aug 9.

Department of Pathology, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, the Netherlands.

The combined fluorescent and Aβ-binding properties of the dietary spice curcumin could yield diagnostic purpose in the search for a non-invasive Aβ-biomarker for Alzheimer's disease (AD). However, evidence on the binding properties of curcumin, its conjugates and clinically used bio-available formulations to AD neuropathological hallmarks is scarce. We therefore assessed the binding properties of different curcumin forms to different neuropathological deposits in post-mortem brain tissue of cases with AD, other neurodegenerative diseases, and controls. Read More

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http://dx.doi.org/10.1186/s40478-018-0577-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6083624PMC
August 2018
15 Reads