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  • 1
    Language: English
    In: Acta neuropathologica, 2016-06, Vol.131 (6), p.803-820
    Description: The 2016 World Health Organization Classification of Tumors of the Central Nervous System is both a conceptual and practical advance over its 2007 predecessor. For the first time, the WHO classification of CNS tumors uses molecular parameters in addition to histology to define many tumor entities, thus formulating a concept for how CNS tumor diagnoses should be structured in the molecular era. As such, the 2016 CNS WHO presents major restructuring of the diffuse gliomas, medulloblastomas and other embryonal tumors, and incorporates new entities that are defined by both histology and molecular features, including glioblastoma, IDH-wildtype and glioblastoma, IDH-mutant; diffuse midline glioma, H3 K27M–mutant; RELA fusion–positive ependymoma; medulloblastoma, WNT-activated and medulloblastoma, SHH-activated; and embryonal tumour with multilayered rosettes, C19MC-altered. The 2016 edition has added newly recognized neoplasms, and has deleted some entities, variants and patterns that no longer have diagnostic and/or biological relevance. Other notable changes include the addition of brain invasion as a criterion for atypical meningioma and the introduction of a soft tissue-type grading system for the now combined entity of solitary fibrous tumor / hemangiopericytoma—a departure from the manner by which other CNS tumors are graded. Overall, it is hoped that the 2016 CNS WHO will facilitate clinical, experimental and epidemiological studies that will lead to improvements in the lives of patients with brain tumors.
    Subject(s): Medicine & Public Health ; Pathology ; Neurosciences ; Central Nervous System Neoplasms - classification ; World Health Organization ; Glioma - classification ; Humans ; Meningioma - classification ; Central Nervous System - pathology ; Meningioma - pathology ; Central Nervous System Neoplasms - pathology ; Animals ; Glioma - pathology ; Brain - pathology ; Meningioma - diagnosis ; Central Nervous System Neoplasms - diagnosis ; Gliomas ; Epidemiology ; Analysis ; Brain tumors ; Public health ; Central nervous system ; Index Medicus ; Life Sciences ; Human health and pathology
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 2
    Language: English
    In: Neurosurgery, 2017-08-01, Vol.81 (2), p.230-239
    Description: Abstract BACKGROUND: Five-aminolevulinic acid (5-ALA) is used for fluorescence-guided resections of malignant glioma at a dose of 20 mg/kg; yet, it is unknown whether lower doses may also provide efficacy. OBJECTIVE: To perform a double-blinded randomized study comparing 3 different doses of 5-ALA. METHODS: Twenty-one patients with suspected malignant glioma were randomly assigned to 0.2, 2, or 20 mg/kg 5-ALA. Investigators were unaware of dose. Intraoperatively, regions of interest were first defined in tumor core, margin, and adjacent white matter under white light. Under violet–blue illumination, the surgeon's impression of fluorescence was recorded per region, followed by spectrometry and biopsy. Plasma was collected after administration and analyzed for 5-ALA and protoporphyrin IX (PPIX) content. RESULTS: The positive predictive value of fluorescence was 100%. Visual and spectrometric fluorescence assessment showed 20 mg/kg to elicit the strongest fluorescence in tumor core and margins, which correlated with cell density. Spectrometric and visual fluorescence correlated significantly. A 10-fold increase in 5-ALA dose (2-20 mg/kg) resulted in a 4-fold increase of fluorescence contrast between marginal tumor and adjacent brain. tmax for 5-ALA was 0.94 h for 20 mg/kg (0.2 kg: 0.50 h, 2 mg/kg: 0.61 h). Integrated PPIX plasma levels were 255.8 and 779.9 mcg*h/l (2 vs 20 mg/kg). Peak plasma concentrations were observed at 1.89 ± 0.71 and 7.83 ± 0.68 h (2 vs 20 mg/kg; average ± Standard Error of Mean [SEM]). CONCLUSION: The highest visible and measurable fluorescence was yielded by 20 mg/kg. No fluorescence was elicited at 0.2 mg/kg. Increasing 5-ALA doses did not result in proportional increases in tissue fluorescence or PPIX accumulation in plasma, indicating that doses higher than 20 mg/kg will not elicit useful increases in fluorescence.
    Subject(s): Plasma ; Index Medicus ; Malignant glioma ; Research—Human—Clinical Trials ; Spectrography ; Randomized study ; Histology ; Aminolevulinic acid ; 5-ALA ; Fluorescence-guided resections
    ISSN: 0148-396X
    E-ISSN: 1524-4040
    Source: Oxford Journals A-Z Archive
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 3
    Language: English
    In: Acta neuropathologica, 2007-08, Vol.114 (2), p.97-109
    Description: The fourth edition of the World Health Organization (WHO) classification of tumours of the central nervous system, published in 2007, lists several new entities, including angiocentric glioma, papillary glioneuronal tumour, rosette-forming glioneuronal tumour of the fourth ventricle, papillary tumour of the pineal region, pituicytoma and spindle cell oncocytoma of the adenohypophysis. Histological variants were added if there was evidence of a different age distribution, location, genetic profile or clinical behaviour; these included pilomyxoid astrocytoma, anaplastic medulloblastoma and medulloblastoma with extensive nodularity. The WHO grading scheme and the sections on genetic profiles were updated and the rhabdoid tumour predisposition syndrome was added to the list of familial tumour syndromes typically involving the nervous system. As in the previous, 2000 edition of the WHO ‘Blue Book’, the classification is accompanied by a concise commentary on clinico-pathological characteristics of each tumour type. The 2007 WHO classification is based on the consensus of an international Working Group of 25 pathologists and geneticists, as well as contributions from more than 70 international experts overall, and is presented as the standard for the definition of brain tumours to the clinical oncology and cancer research communities world-wide.
    Subject(s): Medicine & Public Health ; Pathology ; Central Nervous System Neoplasms - classification ; Humans ; World Health Organization ; Index Medicus ; Review
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 4
    Language: English
    In: BMC cancer, 2009-12-21, Vol.9 (1), p.455-455
    Description: Although primary lymphomas of the central nervous system (PCNSL) and extracerebral diffuse large B-cell lymphoma (DLBCL) cannot be distinguished histologically, it is still a matter of debate whether PCNSL differ from systemic DLBCL with respect to their molecular features and pathogenesis. Analysis of the DNA methylation pattern might provide further data distinguishing these entities at a molecular level. Using an array-based technology we have assessed the DNA methylation status of 1,505 individual CpG loci in five PCNSL and compared the results to DNA methylation profiles of 49 DLBCL and ten hematopoietic controls. We identified 194 genes differentially methylated between PCNSL and normal controls. Interestingly, Polycomb target genes and genes with promoters showing a high CpG content were significantly enriched in the group of genes hypermethylated in PCNSL. However, PCNSL and systemic DLBCL did not differ in their methylation pattern. Based on the data presented here, PCNSL and DLBCL do not differ in their DNA methylation pattern. Thus, DNA methylation analysis does not support a separation of PCNSL and DLBCL into individual entities. However, PCNSL and DLBCL differ in their DNA methylation pattern from non- malignant controls.
    Subject(s): Central Nervous System Neoplasms - metabolism ; Embryonic Stem Cells - metabolism ; Oligonucleotide Array Sequence Analysis - methods ; Central Nervous System Neoplasms - genetics ; Humans ; Gene Expression Regulation, Neoplastic ; Lymphoma - genetics ; Gene Expression Profiling - methods ; Hematopoiesis - genetics ; Polycomb-Group Proteins ; Repressor Proteins - physiology ; Central Nervous System Neoplasms - pathology ; DNA Methylation ; CpG Islands - genetics ; Female ; Repressor Proteins - metabolism ; Cluster Analysis ; Analysis ; DNA ; Central nervous system ; Physiological aspects ; Lymphomas ; Methylation ; Health aspects ; Index Medicus
    ISSN: 1471-2407
    E-ISSN: 1471-2407
    Source: BioMedCentral Open Access
    Source: Academic Search Ultimate
    Source: PubMed Central
    Source: Directory of Open Access Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 5
    Language: English
    In: Acta neuropathologica, 2011-12, Vol.122 (6), p.791-792
    Subject(s): Medicine & Public Health ; Pathology ; Neurosciences ; Lymphoma - physiopathology ; Humans ; Middle Aged ; Male ; CARD Signaling Adaptor Proteins - genetics ; Guanylate Cyclase - physiology ; Toll-Like Receptors - physiology ; Adult ; Female ; Lymphoma - pathology ; Retrospective Studies ; Central Nervous System Neoplasms - physiopathology ; CARD Signaling Adaptor Proteins - physiology ; Central Nervous System Neoplasms - genetics ; Myeloid Differentiation Factor 88 - genetics ; Lymphoma - genetics ; Signal Transduction - genetics ; Mutation - genetics ; Central Nervous System Neoplasms - pathology ; Interleukin-1 Receptor-Associated Kinases - physiology ; Biopsy ; Myeloid Differentiation Factor 88 - physiology ; NF-kappa B - physiology ; Guanylate Cyclase - genetics ; Signal Transduction - physiology ; Aged ; Oncology, Experimental ; Genes ; Genetic research ; Lymphomas ; Genetic aspects ; Research ; Universities and colleges ; Cancer ; Index Medicus
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: Journal of clinical oncology, 2009-12-10, Vol.27 (35), p.5874-5880
    Description: The standard of care for anaplastic gliomas is surgery followed by radiotherapy. The NOA-04 phase III trial compared efficacy and safety of radiotherapy followed by chemotherapy at progression with the reverse sequence in patients with newly diagnosed anaplastic gliomas. Patients (N = 318) were randomly assigned 2:1:1 (A:B1:B2) to receive conventional radiotherapy (arm A); procarbazine, lomustine (CCNU), and vincristine (PCV; arm B1); or temozolomide (arm B2) at diagnosis. At occurrence of unacceptable toxicity or disease progression, patients in arm A were treated with PCV or temozolomide (1:1 random assignment), whereas patients in arms B1 or B2 received radiotherapy. The primary end point was time to treatment failure (TTF), defined as progression after radiotherapy and one chemotherapy in either sequence. Patient characteristics in the intention-to-treat population (n = 274) were balanced between arms. All histologic diagnoses were centrally confirmed. Median TTF (hazard ratio [HR] = 1.2; 95% CI, 0.8 to 1.8), progression-free survival (PFS; HR = 1.0; 95% CI, 0.7 to 1.3, and overall survival (HR = 1.2; 95% CI, 0.8 to 1.9) were similar for arms A and B1/B2. Extent of resection was an important prognosticator. Anaplastic oligodendrogliomas and oligoastrocytomas share the same, better prognosis than anaplastic astrocytomas. Hypermethylation of the O(6)-methylguanine DNA-methyltransferase (MGMT) promoter (HR = 0.59; 95% CI, 0.36 to 1.0), mutations of the isocitrate dehydrogenase (IDH1) gene (HR = 0.48; 95% CI, 0.29 to 0.77), and oligodendroglial histology (HR = 0.33; 95% CI, 0.2 to 0.55) reduced the risk of progression. Hypermethylation of the MGMT promoter was associated with prolonged PFS in the chemotherapy and radiotherapy arm. Initial radiotherapy or chemotherapy achieved comparable results in patients with anaplastic gliomas. IDH1 mutations are a novel positive prognostic factor in anaplastic gliomas, with a favorable impact stronger than that of 1p/19q codeletion or MGMT promoter methylation.
    Subject(s): Procarbazine - administration & dosage ; Dacarbazine - adverse effects ; Antineoplastic Combined Chemotherapy Protocols - administration & dosage ; Humans ; Lomustine - adverse effects ; Middle Aged ; Brain Neoplasms - pathology ; DNA Repair Enzymes - genetics ; Antineoplastic Combined Chemotherapy Protocols - adverse effects ; Male ; Antineoplastic Agents, Alkylating - administration & dosage ; Glioma - radiotherapy ; Glioma - genetics ; Young Adult ; DNA Methylation ; Time Factors ; Radiotherapy, Adjuvant - adverse effects ; Glioma - pathology ; Treatment Failure ; Tumor Suppressor Proteins - genetics ; Dacarbazine - analogs & derivatives ; Vincristine - administration & dosage ; Adult ; Female ; Brain Neoplasms - mortality ; Chemotherapy, Adjuvant ; Brain Neoplasms - radiotherapy ; Promoter Regions, Genetic ; Dacarbazine - administration & dosage ; Glioma - mortality ; Drug Administration Schedule ; Risk Assessment ; Risk Factors ; Kaplan-Meier Estimate ; Proportional Hazards Models ; Brain Neoplasms - genetics ; Isocitrate Dehydrogenase - genetics ; Brain Neoplasms - drug therapy ; Disease Progression ; Disease-Free Survival ; DNA Modification Methylases - genetics ; Procarbazine - adverse effects ; Vincristine - adverse effects ; Aged ; Mutation ; Antineoplastic Agents, Alkylating - adverse effects ; Lomustine - administration & dosage ; Glioma - drug therapy
    ISSN: 0732-183X
    E-ISSN: 1527-7755
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
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  • 7
    Language: English
    In: Acta neuropathologica, 2013-05, Vol.125 (5), p.651-658
    Description: Non-central nervous system hemangiopericytoma (HPC) and solitary fibrous tumor (SFT) are considered by pathologists as two variants of a single tumor entity now subsumed under the entity SFT. Recent detection of frequent NAB2-STAT6 fusions in both, HPC and SFT, provided additional support for this view. On the other hand, current neuropathological practice still distinguishes between HPC and SFT. The present study set out to identify genes involved in the formation of meningeal HPC. We performed exome sequencing and detected the NAB2-STAT6 fusion in DNA of 8/10 meningeal HPC thereby providing evidence of close relationship of these tumors with peripheral SFT. Due to the considerable effort required for exome sequencing, we sought to explore surrogate markers for the NAB2-STAT6 fusion protein. We adopted the Duolink proximity ligation assay and demonstrated the presence of NAB2-STAT6 fusion protein in 17/17 HPC and the absence in 15/15 meningiomas. More practical, presence of the NAB2-STAT6 fusion protein resulted in a strong nuclear signal in STAT6 immunohistochemistry. The nuclear reallocation of STAT6 was detected in 35/37 meningeal HPC and 25/25 meningeal SFT but not in 87 meningiomas representing the most important differential diagnosis. Tissues not harboring the NAB2-STAT6 fusion protein presented with nuclear expression of NAB2 and cytoplasmic expression of STAT6 proteins. In conclusion, we provide strong evidence for meningeal HPC and SFT to constitute variants of a single entity which is defined by NAB2-STAT6 fusion. In addition, we demonstrate that this fusion can be rapidly detected by STAT6 immunohistochemistry which shows a consistent nuclear reallocation. This immunohistochemical assay may prove valuable for the differentiation of HPC and SFT from other mesenchymal neoplasms.
    Subject(s): SFT ; Immunohistochemistry ; Pathology ; Neurosciences ; Medicine & Public Health ; NAB2 ; Proximity ligation ; STAT6 ; Hemangiopericytoma ; Solitary fibrous tumor ; Fusion protein ; Meningioma ; Diagnosis, Differential ; Meningeal Neoplasms - genetics ; Humans ; Hemangiopericytoma - genetics ; Meningeal Neoplasms - diagnosis ; Hemangiopericytoma - metabolism ; RNA, Messenger - metabolism ; Exome ; Oncogene Proteins, Fusion - physiology ; Repressor Proteins - physiology ; STAT6 Transcription Factor - physiology ; Solitary Fibrous Tumors - metabolism ; Meningeal Neoplasms - metabolism ; Solitary Fibrous Tumors - diagnosis ; Hemangiopericytoma - diagnosis ; Solitary Fibrous Tumors - genetics ; Cohort Studies ; Proteins ; Diagnosis ; DNA ; Stem cells ; Tumors ; Index Medicus
    ISSN: 0001-6322
    E-ISSN: 1432-0533
    Source: Alma/SFX Local Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 8
    Language: English
    In: Journal of neuropathology and experimental neurology, 2002-07, Vol.61 (7), p.575-584
    Description: Gangliogliomas represent the most frequent tumor entity in young patients suffering from chronic focal epilepsies. In a series of 326 gangliogliomas collected from the University of Bonn Epilepsy Surgery Program and other departments of neuropathology in Germany, Austria, and Switzerland, epidemiological findings and histopathological hallmarks of gangliogliomas are systematically reviewed. The majority of these tumors occur within the temporal lobe and reveal a biphasic histological architecture characterized by a combination of dysplastic neurons and neoplastic glial cell elements. However, gangliogliomas exhibit a considerable variability in their histopathological appearance. Immunohistochemical studies are an important tool to discriminate these neoplasms from other tumor entities. Almost 80% of gangliogliomas reveal immunoreactivity for CD34, a stem cell epitope not expressed in normal brain. Immunohistochemical reactions for MAP2 or NeuN can be employed to characterize the dysplastic nature of neurons in those areas difficult to discriminate from pre-existing brain parenchyma. Less than 50% of the cases display binucleated neurons. With the frequent finding of “satellite” tumor clusters in adjacent brain regions, gangliogliomas are microscopically less circumscribed than previously assumed. The distinction from diffusely infiltrating gliomas is of considerable importance since tumor recurrence or malignant progression are rare events in gangliogliomas. Only little is known about the molecular pathogenesis of these glioneuronal tumors. Our findings support a dysontogenic origin from a glioneuronal precursor lesion with neoplastic, clonal proliferation of the glial cell population. Candidate genes appear to associate with neurodevelopmental signaling cascades rather than cell cycle control or DNA repair mechanisms. The reelin signaling and tuberin/insulin growth receptor pathways have recently been implicated in ganglioglioma development. Powerful new molecular genetic and biological tools can now be employed to unravel the pathogenesis of these intriguing lesions.
    Subject(s): Neurology ; Biological and medical sciences ; Medical sciences ; Tumors of the nervous system. Phacomatoses ; Antigens, CD34 - metabolism ; Prognosis ; Humans ; Middle Aged ; Brain Neoplasms - pathology ; Brain Neoplasms - physiopathology ; Child, Preschool ; Infant ; Male ; Brain Neoplasms - complications ; Epilepsies, Partial - etiology ; Epilepsies, Partial - physiopathology ; Ganglioglioma - complications ; Anaplasia - physiopathology ; Ganglioglioma - pathology ; Anaplasia - pathology ; Biomarkers, Tumor - metabolism ; Adult ; Female ; Child ; Diagnosis, Differential ; Anaplasia - metabolism ; Epilepsies, Partial - pathology ; Tuberous Sclerosis - genetics ; Tuberous Sclerosis - metabolism ; Tuberous Sclerosis - physiopathology ; Adolescent ; Aged ; Ganglioglioma - physiopathology ; Index Medicus
    ISSN: 0022-3069
    E-ISSN: 1554-6578
    Source: Hellenic Academic Libraries Link
    Source: Oxford Journals 2016 Current and Archive A-Z Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 9
    Language: English
    In: Journal of clinical oncology, 2009-04-01, Vol.27 (10), p.1627-1636
    Description: Medulloblastoma is the most common malignant brain tumor in children. Current treatment decisions are based on clinical variables. Novel tumor-derived biomarkers may improve the risk stratification of medulloblastoma patients. A model for the molecular risk stratification was proposed from an array-based comparative genomic hybridization (array-CGH) screen (n = 80). Fluorescence in situ hybridization (FISH) analyses for chromosome arms 6q, 17p, and 17q and the MYC and MYCN loci were performed in an independent validation set (n = 260). Copy number aberrations were correlated with clinical, histologic, and survival data. Gain of 6q and 17q and genomic amplification of MYC or MYCN were each associated with poor outcome in the array-CGH study (n = 80). In contrast, all patients with 6q-deleted tumors survived. Given these findings, the following hierarchical molecular staging system was defined: (1) MYC/MYCN amplification, (2) 6q gain, (3) 17q gain, (4) 6q and 17q balanced, and (5) 6q deletion. The prognostic value of this staging system was investigated by FISH analysis (n = 260). The addition of molecular markers to clinical risk factors resulted in the identification of a large proportion of patients (72 of 260 patients; 30%) at high risk for relapse and death who would be considered standard risk by application of clinical variables alone. Genomic aberrations in medulloblastoma are powerful independent markers of disease progression and survival. By adding genomic markers to established clinical and histologic variables, outcome prediction can be substantially improved. Because the analyses can be conducted on routine paraffin-embedded material, it will be especially feasible to use this novel molecular staging system in large multicenter clinical trials.
    Subject(s): Oncogene Proteins - genetics ; Prognosis ; Area Under Curve ; Tissue Array Analysis ; Humans ; Cerebellar Neoplasms - mortality ; Kaplan-Meier Estimate ; Child, Preschool ; In Situ Hybridization, Fluorescence ; Male ; Gene Dosage ; Cerebellar Neoplasms - genetics ; Medulloblastoma - mortality ; Chromosomes, Human, Pair 17 - genetics ; Chromosomes, Human, Pair 6 - genetics ; Comparative Genomic Hybridization ; Genes, myc - genetics ; Chromosome Aberrations ; Female ; ROC Curve ; N-Myc Proto-Oncogene Protein ; Medulloblastoma - genetics ; Nuclear Proteins - genetics ; Child ; Index Medicus
    ISSN: 0732-183X
    E-ISSN: 1527-7755
    Source: Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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  • 10
    Language: English
    In: Journal of neuropathology and experimental neurology, 2003-12, Vol.62 (12), p.1287-1301
    Description: Sporadic, late-onset Alzheimer disease (AD) constitutes the most frequent cause of dementia in the elderly population. AD-related pathology is often accompanied by vascular changes. The predominant vascular lesions in AD are cerebral amyloid angiopathy (CAA) and arteriosclerosis/lipohyalinosis (AS/LH). The present study was carried out to examine the coincidence of these small vessel pathologies during the development of cognitive deficits, amyloid β-protein (Aβ) deposition, and neurofibrillary tangle (NFT) formation in sporadic late-onset AD. We correlated the clinical dementia rating (CDR) score, the sequential extension of AD-related Aβ deposition into different parts of the brain, and the extension of NFTs to involve more brain regions with the distribution of CAA and AS/LH in 52 human autopsy brains. The extension of CAA and AS/LH to involve different areas of the brain was associated with a rise of CDR scores and an increase in the extension of Aβ deposition and NFT generation. AD cases showed a higher number of regions with CAA and AS/LH compared to nondemented patients with AD-related pathology and controls. Moreover, we demonstrated a hierarchical sequence in which the different regions of the brain exhibited CAA and AS/LH-affected vessels, allowing the distinction of 3 stages in the development of CAA and AS/LH. The first stage of CAA involved leptomeningeal and neocortical vessels. The second stage was characterized by additional Aβ deposition in allocortical and midbrain vessels. Finally, in a third stage, CAA was observed in the basal ganglia, the thalamus, and in the lower brainstem. In contrast, AS/LH initially affected the basal ganglia in stage A. In stage B this pathology made inroads into the deep white matter, the leptomeningeal arteries of the cortex, the cerebellum, and into the thalamus. Stage C was characterized by AS/LH in brainstem vessels. Our results demonstrate widespread CAA and AS/LH to be associated with the development of cognitive deficits in AD. A combination of both CAA and AS/LH may, therefore, contribute to neurodegeneration in AD. These data also suggest that small vessel disease due to arteriosclerosis and fibro- lipohyalinosis is a potential target for the treatment of AD.
    Subject(s): Neurology ; Biological and medical sciences ; Medical sciences ; Intracranial Arteriosclerosis - pathology ; Alzheimer Disease - physiopathology ; Cognition Disorders - physiopathology ; Cerebral Amyloid Angiopathy - physiopathology ; Humans ; Middle Aged ; Cognition Disorders - pathology ; Male ; Alzheimer Disease - pathology ; Cerebral Amyloid Angiopathy - pathology ; Analysis of Variance ; Aged, 80 and over ; Female ; Aged ; Intracranial Arteriosclerosis - physiopathology ; Index Medicus
    ISSN: 0022-3069
    E-ISSN: 1554-6578
    Source: Hellenic Academic Libraries Link
    Source: Oxford Journals 2016 Current and Archive A-Z Collection
    Source: © ProQuest LLC All rights reserved〈img src="https://exlibris-pub.s3.amazonaws.com/PQ_Logo.jpg" style="vertical-align:middle;margin-left:7px"〉
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