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  • 1
    UID:
    almahu_9948556958602882
    Format: 1 online resource (xiv, 162 pages) : , digital, PDF file(s).
    ISBN: 9781108888202 (ebook)
    Content: An estimated 80 million people live with a neurodegenerative disease. That number is expected to increase rapidly as populations age, lifespans increase, and exposure to toxins rises. Despite decades of research and billions in funding, there are no medications that can slow, much less stop, the progress of these diseases. This is because diseases such as Parkinson's and Alzheimer's do not exist in biology. Yet, hundreds of clinical trials around the world are examining the potential of single therapies in thousands of people sharing one of these labels. Compounding the problem, these therapies were developed on evidence from models that do not come close to capturing the complexity of these diseases in the affected humans. These practices must end. Brain Fables is a call to refocus on understanding living and aging to create the personalized treatments each affected individual desperately needs.
    Note: Title from publisher's bibliographic system (viewed on 29 Jun 2020).
    Additional Edition: Print version: ISBN 9781108744621
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    UID:
    almahu_9948619436602882
    Format: 1 online resource (xv, 179 pages) : , digital, PDF file(s).
    ISBN: 9781108355841 (ebook)
    Series Statement: Cambridge medicine
    Content: Clinical case studies are fundamental in cementing theoretical training, especially for neurological disorders where diagnosis can be difficult. This book describes a variety of clinical scenarios associated with either the misdiagnosis or incorrect management of cognitive and behavioral neurological syndromes, identifying common pitfalls, which are discussed in detail. Each case emphasizes the importance of information derived from the patient's history and physical examination in forming a correct diagnosis. Focusing on disorders and presentations that are a frequent source of confusion, key diagnostic principles are illustrated clearly. Questions to the reader move the narrative along logically, whilst highlighting specific aspects of clinical presentation that lead to the correct diagnosis. Videos of patients connect readers to the cases and demonstrate how to avoid diagnostic pitfalls. An online version of the book can be accessed on Cambridge Core, via the code printed on the inside of the cover.
    Note: Title from publisher's bibliographic system (viewed on 12 Nov 2020).
    Additional Edition: Print version: ISBN 9781108814157
    Language: English
    Keywords: Case Reports
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    UID:
    b3kat_BV027735201
    Format: 1 Online-Ressource
    Edition: [Electronic ed.]
    Note: Electronic ed.: Bonn : FES Library, 2008
    In: Arbeiterwohlfahrt, 1929, 4(1929), H. 11, S. [352]
    Language: Undetermined
    Library Location Call Number Volume/Issue/Year Availability
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  • 4
    Online Resource
    Online Resource
    Amsterdam, Netherlands :Elsevier B.V.,
    UID:
    edoccha_9961017511402883
    Format: 1 online resource (290 pages)
    ISBN: 9780323900645
    Series Statement: Handbook of Clinical Neurology ; v. 192
    Content: Precision Medicine in Neurodegenerative Disorders, Part One, Volume 192 in the Handbook of Clinical Neurology deals with the "Why" in the approach to slow the progression of accelerated brain aging. This volume is intended to provide a scholarly background on the framework, basic science and conceptual pitfalls related to disease-modifying efforts in Parkinson's, Alzheimer's and other neurodegenerative disorders. Among topics covered are different models of precision medicine, the lumping-versus-splitting tension in biomarker development and therapeutics, and the rationale for replacing the convergence of the prevailing autopsy-based nosology of neurodegenerative diseases with the divergence of a systems biology approach to human diseases. Specific chapters are dedicated to the promise of genetic subtypes and the lessons in disease modification offered by the fields of oncology and cystic fibrosis that can be adapted to the field of neurodegeneration. Matching a biology-correcting therapy with those biologically suitable to benefit from such therapy represents the vision and mission of precision medicine, the highest level of personalized medicine.
    Note: Intro -- Precision Medicine in Neurodegenerative Disorders, Part I -- Copyright -- Available titles -- Foreword -- In Memoriam-Michael Parkinson -- Preface -- Contributors -- Contents -- Part 1: Conceptual framework -- Chapter 1: The definition of precision medicine in neurodegenerative disorders and the one disease-many diseases tension -- Introduction -- Lessons from other fields -- Precision Medicine in the Fields of Oncology vs Neurodegeneration -- One Disease-Many Diseases Tension -- Why have we failed in disease modification? -- Disease heterogeneity -- Clinical heterogeneity -- Clinical subtypes -- Data-driven subtypes -- Challenges related to both approaches -- The ``brain-first´´/``body-first´´ hypothesis -- Genetic heterogeneity -- Environmental factors contributing to heterogeneity -- Pathologic heterogeneity -- Other concomitant proteinopathies/concurrent factors -- Pathogenic heterogeneity -- Heterogeneity and the One Disease-Many Diseases Tension -- Requirements for precision medicine -- Biomarkers -- Diagnostic accuracy -- The concept of prodromal stages of neurodegenerative diseases -- Moving From Heterogeneity to Precision Medicine and Successful DMT -- Conclusion -- References -- Chapter 2: Models of precision medicine for neurodegeneration -- From the Clinicopathologic Model to Individualized Biological Subtyping -- Is the Model for Symptomatic Treatments Also Helpful for Precision Medicine? -- The Big Picture -- Logistical Implications of the Clinicopathologic Model of Disease -- The false allure of a perfect trial -- If PD is not one disease, why dont we strategize as if we mean it? -- The epidemiology-therapy disconnect -- Toxic pathology? -- When do we reject a hypothesis? -- ``Lessons from failures´´ -- Why Is There Resistance to Change Away From the Clinicopathology Model?. , Genetic mutations predicting disease mean the corresponding proteins must be toxic -- Absolute values do not tell the story in the way ratios do -- Seeding aggregation assays mean pathology is pathogenic -- Toward a New Model of Precision Medicine -- Biomarker development efforts -- Biomarker-driven molecular subtyping -- Clinical trial efforts -- Conclusions -- Acknowledgment -- Declaration of competing interest -- Disclosures -- Funding -- References -- Chapter 3: Pathology vs pathogenesis: Rationale and pitfalls in the clinicopathology model of neurodegeneration -- Introduction -- Synucleinopathies vs Synucleinopenia -- Clinical phenotypes -- Neuropathology -- Pathological hallmarks -- The question of ``copathology´´ -- From immunohistochemical patterns to ``spread of pathology´´ -- The nonspecificity of Lewy pathology -- The nonpathogenicity of Lewy pathology -- Tau-Based Disorders: Tauopathies vs Tauopenia -- Clinical phenotypes -- Neuropathology -- Pathological hallmarks (Fig. 3.3B) -- On ``copathologies´´ -- Special tau-based cases -- Tau aggregation as consequence, not cause -- The Amyloidosis of Alzheimer's Disease -- Clinical phenotypes -- Neuropathology -- The biomarker-based classification of AD -- Clinicopathologic discrepancies -- Why has tau been considered a more accurate biomarker of AD? -- TDP-43 Proteinopathies and/or TDP-43 Proteinopenia -- Clinical phenotypes -- Neuropathology -- Loss of the soluble TDP-43 has been invisible in research -- Pathology Is Not Pathogenesis -- The biophysics of the transformation of normal protein into pathology -- Conclusions and Future Remarks -- References -- Chapter 4: Mixed pathology as a rule, not exception: Time to reconsider disease nosology -- Introduction -- Tau pathology in the PD brain -- Pathological tau spreading through a ``prion-like´´ mechanism in PD brain. , Interaction between α-synuclein and tau pathogens -- Amyloid plaques deposits in PD brain -- The interaction of amyloid precursor protein and Parkinson's disease associated proteins -- TDP-43 in PD -- Neuroinflammation in the PD Brain -- Pathological α-synuclein may induce neuroinflammation -- Neuroinflammation modulating α-synuclein pathology -- Neuroinflammation participates in α-synuclein propagation -- Possible mechanisms in neuroinflammation-induced PD pathology -- Conclusions -- Acknowledgment -- References -- Chapter 5: Neurodegenerative disorders: From clinicopathology convergence to systems biology divergence -- Introduction -- From GWAS to Disease Pathways -- Systems Medicine for Multifactorial Diseases -- Omics, Multiomics, and Functional Enrichment -- Complex Diseases and Disease Networks -- A Systems Biology View on Parkinson's Disease -- A Systems Biology View on Alzheimer's Disease -- Neurodegeneration Mechanisms From a Systems Biology Point of View -- Concluding Remarks and Perspectives -- References -- Chapter 6: The emergence of genotypic divergence and future precision medicine applications -- A History of Wrong Divergences and Convergences -- Descriptive and Convergent Use of Genetic Variation -- Oligo- and Digenic Genetic Inheritance Causal Quests: First Divergent Steps in Precision Medicine? -- Gain- and Loss-of-Function Genotypes: Truly Divergent Precision Medicine -- Layers of Genotypic Divergence, Penetrance Modifiers, and Somatic Mosaicism -- Penetrance modifiers -- Somatic mosaicism -- Are We Approaching the Limit? -- References -- Chapter 7: Lessons from other fields of medicine, Part 1: Breast cancer -- Introduction to Breast Cancer -- Molecular Subtypes and Evolution of Biomarkers -- Histology -- Endocrine therapy: Estrogen receptor (ER) and progesterone receptor (PR) -- Human epidermal growth factor receptor 2 (HER2). , Surgical Evolution and Multimodal Influences -- Genetics -- Single Gene Prognostic Markers -- Multigene Prognostic Markers -- Future Directions -- Conclusion -- Financial disclosure -- References -- Chapter 8: Lessons from other fields of medicine, Part 2: Cystic fibrosis -- Introduction -- Genetics, Pathophysiology, and Classification -- Novel Therapeutics and Transformation of CF Therapy -- CFTR potentiators -- CFTR correctors -- Turning Back the Clock: Pushing the Age Frontier for CFTR Modulator Therapy -- Translational Read-Through and CFTR mRNA Therapies -- CFTR Biomarkers -- Evolution of Cell-Based Assays and CFTR Modulator Theratyping -- Organizational Support -- Venture philanthropy -- Impact of quality improvement initiatives -- Future of CF Care and Challenges Ahead -- Conclusions -- References -- Chapter 9: Lessons learned from evolving frameworks in adult glioblastoma -- Introduction -- Medical Imaging of GBMs -- Histopathology -- Molecular subtyping -- Transcription-based subtyping -- Early exploration -- The new era -- DNA methylation-based classification -- Genetic alteration-based classification -- Genomic Testing, Diagnosis, and Standard of Care -- Diagnosis -- Prognosis and treatment -- MGMT promoter methylation status -- Surgical treatment -- Molecular subtype-specific therapy -- Clinical Trials and Future Perspectives -- PRMT5 inhibitors -- Therapies targeting CDK5 -- Immunotherapy -- Conclusions -- References -- Further reading -- Part 2: Pitfalls in definitions, cohorts, and measures of progression -- Chapter 10: Finding the falsification threshold of the toxic proteinopathy hypothesis in neurodegeneration -- Background -- Language and narrative -- Belief -- Where is the Threshold of Hypothesis Falsification? -- The foretold conclusion of an unfalsifiable hypothesis: Aducanumab. , The impossible threshold for hypothesis falsification -- Why and How to Falsify a Hypothesis -- It is an ethical imperative that an incorrect hypothesis is falsified -- Underdetermination: Failed hypothesis or failed trial? -- Four steps to falsifying a hypothesis -- Step 1: State the therapeutic hypothesis being tested -- Step 2: Design a simple test of the therapeutic hypothesis -- Step 3: Identify a surrogate marker to rule out background assumptions -- Step 4: Propose an alternative hypothesis (from refutation to rejection) -- An Alternative to the Toxic Proteinopathy Hypothesis -- Conclusions -- References -- Chapter 11: The theoretical problems of ``prodrome´´ and ``phenoconversion´´ in neurodegeneration -- Introduction -- Clinical prodrome -- Dream-enactment behaviors -- Dysautonomia -- Olfactory -- Cognition -- Protein ``propagation´´ as unifying theme between prodrome and disease -- Rationale of and support for the Braak hypothesis of protein propagation -- Lost in translation: ``synucleinopathies´´ -- Lost in translation: ``amyloidopathies´´ -- Lost in translation: ``tauopathies´´ -- Prodrome vs disease and phenoconversion -- Phenoconversion -- Pitfalls in prodromal subtyping -- Purpose of prodromal subtyping -- Suggestions for Future Research -- Conclusions -- Conflict of Interest Disclosures -- References -- Chapter 12: The dilemma between milestones of progression versus clinical scales in Parkinson´s disease -- Introduction -- The Natural History of Parkinson's Disease -- Clinical Scales -- Motor scales -- Motor scale subscores -- Functional and quality of life assessment -- Cognitive scales -- Nonmotor scales -- Wearable technology -- Milestones -- Postural instability -- Medication-related milestones -- Motor complications -- Dementia -- Death -- Discussion -- Conclusion -- Acknowledgments -- References. , Chapter 13: Biomarkers of diagnosis, prognosis, pathogenesis, response to therapy: Convergence or divergence? Lessons fro.
    Additional Edition: Print version: Espay, Alberto J. Precision Medicine in Neurodegenerative Disorders San Diego : Elsevier,c2023 ISBN 9780323855389
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 5
    Online Resource
    Online Resource
    Amsterdam, Netherlands :Elsevier B.V.,
    UID:
    almahu_9949449041502882
    Format: 1 online resource (394 pages)
    ISBN: 9780323900652
    Series Statement: Handbook of Clinical Neurology ; Volume 193
    Content: Precision Medicine in Neurodegenerative Disorders, Part Two, Volume 193 in the Handbook of Clinical Neurology deals with the "How" in the reconfiguration of our approach to slow accelerated brain aging. The book rethinks animal models on which therapies are tested, outlines the progress and expected changes in biological subtyping efforts using lysosomal, endosomal, mitochondrial, immune dysregulation, and inflammatory mechanisms of disease pathophysiology, and the growing role of microbiome in shaping disease. The volume separates the potentially disease-modifying neurorescue and neurorestoration, (e.g., gene therapy and cell replacement therapy) from true precision "medicine"–matching biology with the mechanism of intervention of interest. Specific chapters are dedicated to the promise and challenges of extracellular vesicles for both diagnosis and treatment, the growing application of digital measures and other evaluations of clinical response, the nuts and bolts of novel adaptive clinical trial designs, and the regulatory changes needed to facilitate drug development for disease-modification purposes.
    Additional Edition: Print version: Espay, Alberto J. Precision Medicine in Neurodegenerative Disorders San Diego : Elsevier,c2023 ISBN 9780323855556
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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  • 6
    Online Resource
    Online Resource
    Amsterdam, Netherlands :Elsevier B.V.,
    UID:
    edoccha_9961017316302883
    Format: 1 online resource (394 pages)
    ISBN: 9780323900652
    Series Statement: Handbook of Clinical Neurology ; Volume 193
    Content: Precision Medicine in Neurodegenerative Disorders, Part Two, Volume 193 in the Handbook of Clinical Neurology deals with the "How" in the reconfiguration of our approach to slow accelerated brain aging. The book rethinks animal models on which therapies are tested, outlines the progress and expected changes in biological subtyping efforts using lysosomal, endosomal, mitochondrial, immune dysregulation, and inflammatory mechanisms of disease pathophysiology, and the growing role of microbiome in shaping disease. The volume separates the potentially disease-modifying neurorescue and neurorestoration, (e.g., gene therapy and cell replacement therapy) from true precision "medicine"–matching biology with the mechanism of intervention of interest. Specific chapters are dedicated to the promise and challenges of extracellular vesicles for both diagnosis and treatment, the growing application of digital measures and other evaluations of clinical response, the nuts and bolts of novel adaptive clinical trial designs, and the regulatory changes needed to facilitate drug development for disease-modification purposes.
    Additional Edition: Print version: Espay, Alberto J. Precision Medicine in Neurodegenerative Disorders San Diego : Elsevier,c2023 ISBN 9780323855556
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 7
    Online Resource
    Online Resource
    Amsterdam, Netherlands :Elsevier B.V.,
    UID:
    almahu_9949449041102882
    Format: 1 online resource (290 pages)
    ISBN: 9780323900645
    Series Statement: Handbook of Clinical Neurology ; v. 192
    Content: Precision Medicine in Neurodegenerative Disorders, Part One, Volume 192 in the Handbook of Clinical Neurology deals with the "Why" in the approach to slow the progression of accelerated brain aging. This volume is intended to provide a scholarly background on the framework, basic science and conceptual pitfalls related to disease-modifying efforts in Parkinson's, Alzheimer's and other neurodegenerative disorders. Among topics covered are different models of precision medicine, the lumping-versus-splitting tension in biomarker development and therapeutics, and the rationale for replacing the convergence of the prevailing autopsy-based nosology of neurodegenerative diseases with the divergence of a systems biology approach to human diseases. Specific chapters are dedicated to the promise of genetic subtypes and the lessons in disease modification offered by the fields of oncology and cystic fibrosis that can be adapted to the field of neurodegeneration. Matching a biology-correcting therapy with those biologically suitable to benefit from such therapy represents the vision and mission of precision medicine, the highest level of personalized medicine.
    Note: Intro -- Precision Medicine in Neurodegenerative Disorders, Part I -- Copyright -- Available titles -- Foreword -- In Memoriam-Michael Parkinson -- Preface -- Contributors -- Contents -- Part 1: Conceptual framework -- Chapter 1: The definition of precision medicine in neurodegenerative disorders and the one disease-many diseases tension -- Introduction -- Lessons from other fields -- Precision Medicine in the Fields of Oncology vs Neurodegeneration -- One Disease-Many Diseases Tension -- Why have we failed in disease modification? -- Disease heterogeneity -- Clinical heterogeneity -- Clinical subtypes -- Data-driven subtypes -- Challenges related to both approaches -- The ``brain-first´´/``body-first´´ hypothesis -- Genetic heterogeneity -- Environmental factors contributing to heterogeneity -- Pathologic heterogeneity -- Other concomitant proteinopathies/concurrent factors -- Pathogenic heterogeneity -- Heterogeneity and the One Disease-Many Diseases Tension -- Requirements for precision medicine -- Biomarkers -- Diagnostic accuracy -- The concept of prodromal stages of neurodegenerative diseases -- Moving From Heterogeneity to Precision Medicine and Successful DMT -- Conclusion -- References -- Chapter 2: Models of precision medicine for neurodegeneration -- From the Clinicopathologic Model to Individualized Biological Subtyping -- Is the Model for Symptomatic Treatments Also Helpful for Precision Medicine? -- The Big Picture -- Logistical Implications of the Clinicopathologic Model of Disease -- The false allure of a perfect trial -- If PD is not one disease, why dont we strategize as if we mean it? -- The epidemiology-therapy disconnect -- Toxic pathology? -- When do we reject a hypothesis? -- ``Lessons from failures´´ -- Why Is There Resistance to Change Away From the Clinicopathology Model?. , Genetic mutations predicting disease mean the corresponding proteins must be toxic -- Absolute values do not tell the story in the way ratios do -- Seeding aggregation assays mean pathology is pathogenic -- Toward a New Model of Precision Medicine -- Biomarker development efforts -- Biomarker-driven molecular subtyping -- Clinical trial efforts -- Conclusions -- Acknowledgment -- Declaration of competing interest -- Disclosures -- Funding -- References -- Chapter 3: Pathology vs pathogenesis: Rationale and pitfalls in the clinicopathology model of neurodegeneration -- Introduction -- Synucleinopathies vs Synucleinopenia -- Clinical phenotypes -- Neuropathology -- Pathological hallmarks -- The question of ``copathology´´ -- From immunohistochemical patterns to ``spread of pathology´´ -- The nonspecificity of Lewy pathology -- The nonpathogenicity of Lewy pathology -- Tau-Based Disorders: Tauopathies vs Tauopenia -- Clinical phenotypes -- Neuropathology -- Pathological hallmarks (Fig. 3.3B) -- On ``copathologies´´ -- Special tau-based cases -- Tau aggregation as consequence, not cause -- The Amyloidosis of Alzheimer's Disease -- Clinical phenotypes -- Neuropathology -- The biomarker-based classification of AD -- Clinicopathologic discrepancies -- Why has tau been considered a more accurate biomarker of AD? -- TDP-43 Proteinopathies and/or TDP-43 Proteinopenia -- Clinical phenotypes -- Neuropathology -- Loss of the soluble TDP-43 has been invisible in research -- Pathology Is Not Pathogenesis -- The biophysics of the transformation of normal protein into pathology -- Conclusions and Future Remarks -- References -- Chapter 4: Mixed pathology as a rule, not exception: Time to reconsider disease nosology -- Introduction -- Tau pathology in the PD brain -- Pathological tau spreading through a ``prion-like´´ mechanism in PD brain. , Interaction between α-synuclein and tau pathogens -- Amyloid plaques deposits in PD brain -- The interaction of amyloid precursor protein and Parkinson's disease associated proteins -- TDP-43 in PD -- Neuroinflammation in the PD Brain -- Pathological α-synuclein may induce neuroinflammation -- Neuroinflammation modulating α-synuclein pathology -- Neuroinflammation participates in α-synuclein propagation -- Possible mechanisms in neuroinflammation-induced PD pathology -- Conclusions -- Acknowledgment -- References -- Chapter 5: Neurodegenerative disorders: From clinicopathology convergence to systems biology divergence -- Introduction -- From GWAS to Disease Pathways -- Systems Medicine for Multifactorial Diseases -- Omics, Multiomics, and Functional Enrichment -- Complex Diseases and Disease Networks -- A Systems Biology View on Parkinson's Disease -- A Systems Biology View on Alzheimer's Disease -- Neurodegeneration Mechanisms From a Systems Biology Point of View -- Concluding Remarks and Perspectives -- References -- Chapter 6: The emergence of genotypic divergence and future precision medicine applications -- A History of Wrong Divergences and Convergences -- Descriptive and Convergent Use of Genetic Variation -- Oligo- and Digenic Genetic Inheritance Causal Quests: First Divergent Steps in Precision Medicine? -- Gain- and Loss-of-Function Genotypes: Truly Divergent Precision Medicine -- Layers of Genotypic Divergence, Penetrance Modifiers, and Somatic Mosaicism -- Penetrance modifiers -- Somatic mosaicism -- Are We Approaching the Limit? -- References -- Chapter 7: Lessons from other fields of medicine, Part 1: Breast cancer -- Introduction to Breast Cancer -- Molecular Subtypes and Evolution of Biomarkers -- Histology -- Endocrine therapy: Estrogen receptor (ER) and progesterone receptor (PR) -- Human epidermal growth factor receptor 2 (HER2). , Surgical Evolution and Multimodal Influences -- Genetics -- Single Gene Prognostic Markers -- Multigene Prognostic Markers -- Future Directions -- Conclusion -- Financial disclosure -- References -- Chapter 8: Lessons from other fields of medicine, Part 2: Cystic fibrosis -- Introduction -- Genetics, Pathophysiology, and Classification -- Novel Therapeutics and Transformation of CF Therapy -- CFTR potentiators -- CFTR correctors -- Turning Back the Clock: Pushing the Age Frontier for CFTR Modulator Therapy -- Translational Read-Through and CFTR mRNA Therapies -- CFTR Biomarkers -- Evolution of Cell-Based Assays and CFTR Modulator Theratyping -- Organizational Support -- Venture philanthropy -- Impact of quality improvement initiatives -- Future of CF Care and Challenges Ahead -- Conclusions -- References -- Chapter 9: Lessons learned from evolving frameworks in adult glioblastoma -- Introduction -- Medical Imaging of GBMs -- Histopathology -- Molecular subtyping -- Transcription-based subtyping -- Early exploration -- The new era -- DNA methylation-based classification -- Genetic alteration-based classification -- Genomic Testing, Diagnosis, and Standard of Care -- Diagnosis -- Prognosis and treatment -- MGMT promoter methylation status -- Surgical treatment -- Molecular subtype-specific therapy -- Clinical Trials and Future Perspectives -- PRMT5 inhibitors -- Therapies targeting CDK5 -- Immunotherapy -- Conclusions -- References -- Further reading -- Part 2: Pitfalls in definitions, cohorts, and measures of progression -- Chapter 10: Finding the falsification threshold of the toxic proteinopathy hypothesis in neurodegeneration -- Background -- Language and narrative -- Belief -- Where is the Threshold of Hypothesis Falsification? -- The foretold conclusion of an unfalsifiable hypothesis: Aducanumab. , The impossible threshold for hypothesis falsification -- Why and How to Falsify a Hypothesis -- It is an ethical imperative that an incorrect hypothesis is falsified -- Underdetermination: Failed hypothesis or failed trial? -- Four steps to falsifying a hypothesis -- Step 1: State the therapeutic hypothesis being tested -- Step 2: Design a simple test of the therapeutic hypothesis -- Step 3: Identify a surrogate marker to rule out background assumptions -- Step 4: Propose an alternative hypothesis (from refutation to rejection) -- An Alternative to the Toxic Proteinopathy Hypothesis -- Conclusions -- References -- Chapter 11: The theoretical problems of ``prodrome´´ and ``phenoconversion´´ in neurodegeneration -- Introduction -- Clinical prodrome -- Dream-enactment behaviors -- Dysautonomia -- Olfactory -- Cognition -- Protein ``propagation´´ as unifying theme between prodrome and disease -- Rationale of and support for the Braak hypothesis of protein propagation -- Lost in translation: ``synucleinopathies´´ -- Lost in translation: ``amyloidopathies´´ -- Lost in translation: ``tauopathies´´ -- Prodrome vs disease and phenoconversion -- Phenoconversion -- Pitfalls in prodromal subtyping -- Purpose of prodromal subtyping -- Suggestions for Future Research -- Conclusions -- Conflict of Interest Disclosures -- References -- Chapter 12: The dilemma between milestones of progression versus clinical scales in Parkinson´s disease -- Introduction -- The Natural History of Parkinson's Disease -- Clinical Scales -- Motor scales -- Motor scale subscores -- Functional and quality of life assessment -- Cognitive scales -- Nonmotor scales -- Wearable technology -- Milestones -- Postural instability -- Medication-related milestones -- Motor complications -- Dementia -- Death -- Discussion -- Conclusion -- Acknowledgments -- References. , Chapter 13: Biomarkers of diagnosis, prognosis, pathogenesis, response to therapy: Convergence or divergence? Lessons fro.
    Additional Edition: Print version: Espay, Alberto J. Precision Medicine in Neurodegenerative Disorders San Diego : Elsevier,c2023 ISBN 9780323855389
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 8
    Online Resource
    Online Resource
    Amsterdam, Netherlands :Elsevier B.V.,
    UID:
    edocfu_9961017316302883
    Format: 1 online resource (394 pages)
    ISBN: 9780323900652
    Series Statement: Handbook of Clinical Neurology ; Volume 193
    Content: Precision Medicine in Neurodegenerative Disorders, Part Two, Volume 193 in the Handbook of Clinical Neurology deals with the "How" in the reconfiguration of our approach to slow accelerated brain aging. The book rethinks animal models on which therapies are tested, outlines the progress and expected changes in biological subtyping efforts using lysosomal, endosomal, mitochondrial, immune dysregulation, and inflammatory mechanisms of disease pathophysiology, and the growing role of microbiome in shaping disease. The volume separates the potentially disease-modifying neurorescue and neurorestoration, (e.g., gene therapy and cell replacement therapy) from true precision "medicine"–matching biology with the mechanism of intervention of interest. Specific chapters are dedicated to the promise and challenges of extracellular vesicles for both diagnosis and treatment, the growing application of digital measures and other evaluations of clinical response, the nuts and bolts of novel adaptive clinical trial designs, and the regulatory changes needed to facilitate drug development for disease-modification purposes.
    Additional Edition: Print version: Espay, Alberto J. Precision Medicine in Neurodegenerative Disorders San Diego : Elsevier,c2023 ISBN 9780323855556
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 9
    UID:
    b3kat_BV027698205
    In: Arbeiterwohlfahrt, 1929, 4(1929), H. 11, S. [352]
    Language: Undetermined
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 10
    Book
    Book
    Philadelphia, Pa. [u.a.] :Wolters Kluwer, Lippincott Williams & Wilkins,
    UID:
    almafu_BV037379599
    Format: XXI, 370 S. : , Ill., graph. Darst. ; , 23 cm.
    ISBN: 978-1-4511-1360-0 , 1-4511-1360-9
    Language: English
    Library Location Call Number Volume/Issue/Year Availability
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