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  1. Article: "Biomarker kann man bald nicht mehr ignorieren". Interview mit Prof. Dr. Harald Hampel zur Alzheimerdiagnostik

    Hampel, Harald

    Der Neurologe & Psychiater

    2012  Volume 13, Issue 3, Page(s) 18

    Language German
    Document type Article
    ZDB-ID 2036795-8
    ISSN 1616-2455
    Database Current Contents Medicine

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5588: Show issues Location:
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  2. Book: Alzheimer's disease - modernizing concept, biological diagnosis and therapy

    Hampel, Harald / Carillo, Maria C.

    14 tables

    (Advances in biological psychiatry ; 28)

    2012  

    Author's details vol. ed.: H. Hampel ; M. C. Carillo
    Series title Advances in biological psychiatry ; 28
    Collection
    Keywords Alzheimerkrankheit
    Subject Alzheimer-Krankheit ; Alzheimersche Krankheit ; Alzheimer-Demenz ; Morbus Alzheimer ; Greisenblödsinn ; Alzheimer's Disease
    Language English
    Size V, 193 S. : Ill., graph. Darst.
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT017217127
    ISBN 978-3-8055-9802-6 ; 3-8055-9802-5 ; 9783805598033 ; 3805598033
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2012 A 2480 order for loan Magazin

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  3. Book: Alzheimer-Demenz

    Auer, Stefanie / Hampel, Harald

    klinische Verläufe, diagnostische Möglichkeiten, moderne Therapiestrategien

    2003  

    Author's details hrsg. von Harald Hampel ... Unter Mitarbeit von S. Auer
    Keywords Alzheimerkrankheit
    Subject Alzheimer-Krankheit ; Alzheimersche Krankheit ; Alzheimer-Demenz ; Morbus Alzheimer ; Greisenblödsinn ; Alzheimer's Disease
    Language German
    Size IX, 500 S. : Ill., graph. Darst.
    Publisher Wiss. Verl.-Ges
    Publishing place Stuttgart
    Publishing country Germany
    Document type Book
    HBZ-ID HT013577902
    ISBN 3-8047-1928-7 ; 978-3-8047-1928-6
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2003 A 653 order for loan Magazin

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  4. Article ; Online: Reversible C═N Bond Formation Controls Charge-Separation in an Aza-Diarylethene Photoswitch.

    Sacherer, Maximilian / Gracheva, Sofia / Maid, Harald / Placht, Christian / Hampel, Frank / Dube, Henry

    Journal of the American Chemical Society

    2024  Volume 146, Issue 14, Page(s) 9575–9582

    Abstract: Diarylethenes belong to the most eminent photoswitches and have been studied for many decades. They are found in virtually every field of application and have become highly valuable molecular tools for instilling light-responsiveness into materials, ... ...

    Abstract Diarylethenes belong to the most eminent photoswitches and have been studied for many decades. They are found in virtually every field of application and have become highly valuable molecular tools for instilling light-responsiveness into materials, catalysts, biological systems, or pharmacology. In this work, we present a novel and distinct type of pyrimidine-based aza-diarylethene, which undergoes a highly unusual zwitterion-forming photoreaction. During this fully reversible process, a CN double bond is established under concomitant aromatization and thiophene-ring opening. The metastable zwitterion thus possesses a positively charged extended aromatic structure and an independent conjugated thiolate function. It can further photoisomerize between a more stable
    Language English
    Publishing date 2024-03-27
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3155-0
    ISSN 1520-5126 ; 0002-7863
    ISSN (online) 1520-5126
    ISSN 0002-7863
    DOI 10.1021/jacs.3c11803
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Bonn / Germany

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  5. Book ; Thesis: Ein- und zweidimensionale Gelelektrophorese von postmortalem zerebralem Gewebe bei schizophrenen Erkrankungen

    Hampel, Harald

    Nachweis immunomodulatorisch wirksamer Proteine

    1995  

    Author's details vorgelegt von Harald-Jürgen Hampel
    Language German
    Size IV, 125 S. : Ill.
    Document type Book ; Thesis
    Thesis / German Habilitation thesis München, Univ., Diss., 1996
    HBZ-ID HT007375356
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    96 D 3753 order for loan Magazin

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  6. Book ; Online ; Thesis: Auswirkungen des flexiblen Betriebs von Luftzerlegungsanlagen auf den Hauptwärmeübertrager

    Fritsch, Philipp Maximilian Verfasser] / [Klein, Harald [Akademischer Betreuer] / Hampel, Uwe Gutachter] / [Klein, Harald [Gutachter]

    2022  

    Author's details Philipp Maximilian Fritsch ; Gutachter: Uwe Hampel, Harald Klein ; Betreuer: Harald Klein
    Keywords Technische Chemie ; Technical Chemistry
    Subject code sg660
    Language German
    Publisher Universitätsbibliothek der TU München
    Publishing place München
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

    Full text online

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  7. Book ; Online ; Thesis: Experimental and Numerical Investigations for an Advanced Modeling of Two-Phase Flow and Mass Transfer on Column Trays

    Vishwakarma, Vineet [Verfasser] / Hampel, Uwe [Gutachter] / Klein, Harald [Gutachter]

    2022  

    Author's details Vineet Vishwakarma ; Gutachter: Uwe Hampel, Harald Klein
    Keywords Technische Chemie ; Technical Chemistry
    Subject code sg660
    Language English
    Publisher Technische Universität Dresden
    Publishing place Dresden
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

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  8. Article ; Online: Amyloid-related imaging abnormalities (ARIA): radiological, biological and clinical characteristics.

    Hampel, Harald / Elhage, Aya / Cho, Min / Apostolova, Liana G / Nicoll, James A R / Atri, Alireza

    Brain : a journal of neurology

    2023  Volume 146, Issue 11, Page(s) 4414–4424

    Abstract: Excess accumulation and aggregation of toxic soluble and insoluble amyloid-β species in the brain are a major hallmark of Alzheimer's disease. Randomized clinical trials show reduced brain amyloid-β deposits using monoclonal antibodies that target ... ...

    Abstract Excess accumulation and aggregation of toxic soluble and insoluble amyloid-β species in the brain are a major hallmark of Alzheimer's disease. Randomized clinical trials show reduced brain amyloid-β deposits using monoclonal antibodies that target amyloid-β and have identified MRI signal abnormalities called amyloid-related imaging abnormalities (ARIA) as possible spontaneous or treatment-related adverse events. This review provides a comprehensive state-of-the-art conceptual review of radiological features, clinical detection and classification challenges, pathophysiology, underlying biological mechanism(s) and risk factors/predictors associated with ARIA. We summarize the existing literature and current lines of evidence with ARIA-oedema/effusion (ARIA-E) and ARIA-haemosiderosis/microhaemorrhages (ARIA-H) seen across anti-amyloid clinical trials and therapeutic development. Both forms of ARIA may occur, often early, during anti-amyloid-β monoclonal antibody treatment. Across randomized controlled trials, most ARIA cases were asymptomatic. Symptomatic ARIA-E cases often occurred at higher doses and resolved within 3-4 months or upon treatment cessation. Apolipoprotein E haplotype and treatment dosage are major risk factors for ARIA-E and ARIA-H. Presence of any microhaemorrhage on baseline MRI increases the risk of ARIA. ARIA shares many clinical, biological and pathophysiological features with Alzheimer's disease and cerebral amyloid angiopathy. There is a great need to conceptually link the evident synergistic interplay associated with such underlying conditions to allow clinicians and researchers to further understand, deliberate and investigate on the combined effects of these multiple pathophysiological processes. Moreover, this review article aims to better assist clinicians in detection (either observed via symptoms or visually on MRI), management based on appropriate use recommendations, and general preparedness and awareness when ARIA are observed as well as researchers in the fundamental understanding of the various antibodies in development and their associated risks of ARIA. To facilitate ARIA detection in clinical trials and clinical practice, we recommend the implementation of standardized MRI protocols and rigorous reporting standards. With the availability of approved amyloid-β therapies in the clinic, standardized and rigorous clinical and radiological monitoring and management protocols are required to effectively detect, monitor, and manage ARIA in real-world clinical settings.
    MeSH term(s) Humans ; Alzheimer Disease/complications ; Antibodies, Monoclonal, Humanized/therapeutic use ; Amyloid beta-Peptides/metabolism ; Brain/metabolism ; Amyloid ; Amyloidogenic Proteins
    Chemical Substances Antibodies, Monoclonal, Humanized ; Amyloid beta-Peptides ; Amyloid ; Amyloidogenic Proteins
    Language English
    Publishing date 2023-06-09
    Publishing country England
    Document type Review ; Journal Article
    ZDB-ID 80072-7
    ISSN 1460-2156 ; 0006-8950
    ISSN (online) 1460-2156
    ISSN 0006-8950
    DOI 10.1093/brain/awad188
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ui II Zs.26: Show issues Location:
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  9. Article ; Online: Amyloid-β and cognition in aging and Alzheimer's disease: molecular and neurophysiological mechanisms.

    Hampel, Harald

    Journal of Alzheimer's disease : JAD

    2013  Volume 33 Suppl 1, Page(s) S79–86

    Abstract: Amyloid-β (Aβ) deposition in the brain is one of the key pathological features of Alzheimer's disease (AD). Neither traditional clinical-pathological studies nor modern in vivo biomarker investigations of brain amyloid load, however, could reveal a ... ...

    Abstract Amyloid-β (Aβ) deposition in the brain is one of the key pathological features of Alzheimer's disease (AD). Neither traditional clinical-pathological studies nor modern in vivo biomarker investigations of brain amyloid load, however, could reveal a convincing relationship between brain Aβ load and cognitive deficits and decline in patients with AD. Evidence suggests that pathophysiological Aβ dysregulation and accumulation are very early events that precede the onset of cognitive impairment reaching a plateau at the clinical stage of the beginning dementia syndrome. Therefore, research efforts have focused on the role of Aβ in asymptomatic older adults: the results of combined amyloid-PET and neuropsychological studies show a modest but significant correlation between brain fibrillar amyloid load and various subtle cognitive deficits, most notably in challenging episodic associative memory tasks. In order to elucidate the pathophysiological link between cognition and Aβ, a number of combined functional neuroimaging studies have been performed, resulting in early and complex functional alterations in cognitively relevant neural networks such as the default mode network and the largely overlapping episodic memory networks. Multimodal studies using amyloid-tracing imaging methods and neurodegeneration biomarkers strongly suggest that neural network discoordination is specifically related to Aβ-mediated functional and potentially reversible disruption of synaptic plasticity rather than a direct consequence to neurodegenerative pathological processes. These pathophysiological processes and mechanisms may dynamically and non-linearly evolve through fully reversible adaptive compensatory stages and through reactive decompensatory stages into fully irreversible neurodegenerative stages of AD.
    MeSH term(s) Aging/metabolism ; Aging/pathology ; Aging/psychology ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/metabolism ; Alzheimer Disease/pathology ; Alzheimer Disease/psychology ; Amyloid beta-Peptides/metabolism ; Brain/diagnostic imaging ; Brain/metabolism ; Brain/pathology ; Cognition ; Cognition Disorders/diagnostic imaging ; Cognition Disorders/metabolism ; Cognition Disorders/pathology ; Cognition Disorders/psychology ; Humans ; Radionuclide Imaging
    Chemical Substances Amyloid beta-Peptides
    Language English
    Publishing date 2013
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-2012-129003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6084: Show issues Location:
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  10. Article ; Online: Pyridinic Nanographenes by Novel Precursor Design.

    Reger, David / Schöll, Kilian / Hampel, Frank / Maid, Harald / Jux, Norbert

    Chemistry (Weinheim an der Bergstrasse, Germany)

    2021  Volume 27, Issue 6, Page(s) 1984–1989

    Abstract: In this work we present the solution-synthesis of pyridine analogues to hexa-peri-hexabenzocoronene (HBC)-which might be called superpyridines-via a novel precursor design. The key step in our strategy was the pre-formation of the C-C bonds between the 3/ ...

    Abstract In this work we present the solution-synthesis of pyridine analogues to hexa-peri-hexabenzocoronene (HBC)-which might be called superpyridines-via a novel precursor design. The key step in our strategy was the pre-formation of the C-C bonds between the 3/3' positions of the pyridine and the adjacent phenyl rings-bonds that are otherwise unreactive and difficult to close under Scholl-conditions. Apart from the synthesis of the parent compound we show that classical pyridine chemistry, namely oxidation, N-alkylation and metal-coordination is applicable to the π-extended analogue. Furthermore, we present basic physical chemical characterizations of the newly synthesized molecules. With this novel synthetic strategy, we hope to unlock the pyridine chemistry of nanographenes.
    Language English
    Publishing date 2021-01-12
    Publishing country Germany
    Document type Journal Article
    ZDB-ID 1478547-X
    ISSN 1521-3765 ; 0947-6539
    ISSN (online) 1521-3765
    ISSN 0947-6539
    DOI 10.1002/chem.202004983
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