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  1. 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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  2. 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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  3. 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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  4. 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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  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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  6. Article ; Online: Current insights into the pathophysiology of Alzheimer's disease: selecting targets for early therapeutic intervention.

    Hampel, Harald

    International psychogeriatrics

    2012  Volume 24 Suppl 1, Page(s) S10–7

    Abstract: The development of therapies for Alzheimer's disease (AD) presents numerous challenges for physicians, researchers, and the pharmaceutical industry, with many drug candidates showing promise at one stage of clinical research only to fall at the next ... ...

    Abstract The development of therapies for Alzheimer's disease (AD) presents numerous challenges for physicians, researchers, and the pharmaceutical industry, with many drug candidates showing promise at one stage of clinical research only to fall at the next hurdle. A great number of drugs with a variety of targets and clusters of mechanisms are currently in various stages of basic and clinical investigation. However, these hypothesis-derived agents may be tested much too late in the chronically progressive disease process to demonstrate meaningful effects or outcomes, mirroring the clinical syndromal scenario in which the underlying pathophysiological disease condition is frequently diagnosed extremely late. Moreover, the complexity of the disease calls for developments and improvements in study designs and methods modeled for different target populations and disease stages (e.g. asymptomatic to prodromal to syndromal). New integrated concepts and models of disease pathophysiology, use of validated and qualified biomarkers, outcomes and endpoints, particularly the development of a surrogate outcome, may allow targeting of characteristic mechanism-derived therapies of specifically affected biological systems at different time-points in the disease process, providing increasing opportunities for early and preventative intervention. A core set of feasible diagnostic and predictive biomarkers is already validated and in the process of standardization; however, continued and intensified research efforts will likely reveal a variety of novel biomarkers that grasp the complexity of the underlying disease process. In the future, trials of drugs to modify and prevent AD may embrace enrichment strategies and maybe be stratified by disease stage, genetic factors as well as by disease endophenotypes.
    MeSH term(s) Alzheimer Disease/drug therapy ; Alzheimer Disease/physiopathology ; Alzheimer Disease/prevention & control ; Biomarkers/analysis ; Disease Progression ; Ginkgo biloba ; Humans ; Phytotherapy ; Plant Extracts/therapeutic use
    Chemical Substances Biomarkers ; Plant Extracts ; Ginkgo biloba extract (19FUJ2C58T)
    Language English
    Publishing date 2012-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1038825-4
    ISSN 1741-203X ; 1041-6102
    ISSN (online) 1741-203X
    ISSN 1041-6102
    DOI 10.1017/S1041610212000579
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Book ; Online: Alzheimer's Disease - Modernizing Concept, Biological Diagnosis and Therapy

    Hampel, Harald

    (Advances in Biological Psychiatry ; 28)

    2012  

    Author's details H. Hampel ... (vol. eds.)
    Series title Advances in Biological Psychiatry ; 28
    Language English
    Size 1 Online-Ressource (VI, 194 S)
    Document type Book ; Online
    Note How current biomarkers are modernizing the diagnosis of Alzheimer's disease
    ISBN 9783805598026 ; 9783805598033 ; 3805598025 ; 3805598033
    Database Special collection on veterinary medicine and general parasitology

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  8. Article: A Systematic Review of Clinical Practice Guidelines for Alzheimer's Disease and Strategies for Future Advancements.

    Tahami Monfared, Amir Abbas / Phan, N T Nhan / Pearson, Isobel / Mauskopf, Josephine / Cho, Min / Zhang, Quanwu / Hampel, Harald

    Neurology and therapy

    2023  Volume 12, Issue 4, Page(s) 1257–1284

    Abstract: Introduction: Alzheimer's disease (AD) is a disease continuum from pathophysiologic, biomarker and clinical perspectives. With the advent of advanced technologies, diagnosing and managing patients is evolving.: Methods: A systematic literature review ...

    Abstract Introduction: Alzheimer's disease (AD) is a disease continuum from pathophysiologic, biomarker and clinical perspectives. With the advent of advanced technologies, diagnosing and managing patients is evolving.
    Methods: A systematic literature review (SLR) of practice guidelines for mild cognitive impairment (MCI) and AD dementia was performed following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). This systematic literature review (SLR) aimed to summarize current clinical practice guidelines for screening, testing, diagnosis, treatment and monitoring in the AD continuum. The results of this SLR were used to propose a way forward for practice guidelines given the possible introduction of biomarker-guided technology using blood- or plasma-based assays and disease-modifying treatments (DMTs) targeted for early disease.
    Results: 53 clinical practice guidelines were identified, 15 of which were published since 2018. Screening for asymptomatic populations was not recommended. Biomarker testing was not included in routine diagnostic practice. There was no consensus on which neurocognitive tests to use to diagnose and monitor MCI or AD dementia. Pharmacologic therapies were not recommended for MCI, while cholinesterase inhibitors and memantine were recommended for AD treatment.
    Discussion: The pre-2018 and post-2018 practice guidelines share similar recommendations for screening, diagnosis and treatment. However, once DMTs are approved, clinicians will require guidance on the appropriate use of DMTs in a clinical setting. This guidance should include strategies for identifying eligible patients and evaluating the DMT benefit-to-risk profile to facilitate shared decision-making among physicians, patients and care partners.
    Conclusion: Regular evidence-based updates of existing guidelines for the AD continuum are required over the coming decades to integrate rapidly evolving technologic and medical scientific advances and bring emerging approaches for management of early disease into clinical practice. This will pave the way toward biomarker-guided identification and targeted treatment and the realization of precision medicine for AD.
    Language English
    Publishing date 2023-06-01
    Publishing country New Zealand
    Document type Journal Article
    ISSN 2193-8253
    ISSN 2193-8253
    DOI 10.1007/s40120-023-00504-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: The foundation and architecture of precision medicine in neurology and psychiatry.

    Hampel, Harald / Gao, Peng / Cummings, Jeffrey / Toschi, Nicola / Thompson, Paul M / Hu, Yan / Cho, Min / Vergallo, Andrea

    Trends in neurosciences

    2023  Volume 46, Issue 3, Page(s) 176–198

    Abstract: Neurological and psychiatric diseases have high degrees of genetic and pathophysiological heterogeneity, irrespective of clinical manifestations. Traditional medical paradigms have focused on late-stage syndromic aspects of these diseases, with little ... ...

    Abstract Neurological and psychiatric diseases have high degrees of genetic and pathophysiological heterogeneity, irrespective of clinical manifestations. Traditional medical paradigms have focused on late-stage syndromic aspects of these diseases, with little consideration of the underlying biology. Advances in disease modeling and methodological design have paved the way for the development of precision medicine (PM), an established concept in oncology with growing attention from other medical specialties. We propose a PM architecture for central nervous system diseases built on four converging pillars: multimodal biomarkers, systems medicine, digital health technologies, and data science. We discuss Alzheimer's disease (AD), an area of significant unmet medical need, as a case-in-point for the proposed framework. AD can be seen as one of the most advanced PM-oriented disease models and as a compelling catalyzer towards PM-oriented neuroscience drug development and advanced healthcare practice.
    MeSH term(s) Humans ; Precision Medicine ; Alzheimer Disease ; Neurology ; Neurosciences ; Psychiatry
    Language English
    Publishing date 2023-01-13
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 282488-7
    ISSN 1878-108X ; 0378-5912 ; 0166-2236
    ISSN (online) 1878-108X
    ISSN 0378-5912 ; 0166-2236
    DOI 10.1016/j.tins.2022.12.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Synaptic degeneration and neurogranin in the pathophysiology of Alzheimer's disease.

    Lista, Simone / Hampel, Harald

    Expert review of neurotherapeutics

    2017  Volume 17, Issue 1, Page(s) 47–57

    Abstract: Introduction: Synaptic dysfunction and degeneration are early fundamental pathophysiological characteristics of Alzheimer's disease (AD). In addition, synaptic depletion closely correlates with clinical disease severity. Biomarkers that may track ... ...

    Abstract Introduction: Synaptic dysfunction and degeneration are early fundamental pathophysiological characteristics of Alzheimer's disease (AD). In addition, synaptic depletion closely correlates with clinical disease severity. Biomarkers that may track synaptic dysfunction in AD are eagerly awaited. Areas covered: Here, we reviewed the significance of the post-synaptic protein neurogranin - particularly enriched in dendritic spines - as a biomarker of early synaptic dysfunction in AD. We also examined its role as a marker to predict disease progression. Expert commentary: Current evidence indicates that neurogranin may serve as a mechanism-of-action biomarker aiding the in vivo investigation of AD-related pathophysiological pathways. Its use may support the development of targeted therapeutic interventions tailored to the individual patient, i.e. 'molecularly' targeted therapies, according to the evolving precision medicine paradigm.
    MeSH term(s) Alzheimer Disease/metabolism ; Alzheimer Disease/physiopathology ; Amyloid beta-Peptides/metabolism ; Biomarkers ; Disease Progression ; Humans ; Neurogranin
    Chemical Substances Amyloid beta-Peptides ; Biomarkers ; Neurogranin (132654-77-4)
    Language English
    Publishing date 2017-01
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2112534-X
    ISSN 1744-8360 ; 1473-7175
    ISSN (online) 1744-8360
    ISSN 1473-7175
    DOI 10.1080/14737175.2016.1204234
    Database MEDical Literature Analysis and Retrieval System OnLINE

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