Details

Autor(en) / Beteiligte

• Prajapati, Bhupendra,
• Chellappan, Dinesh Kumar,
• Kendre, Prakash,

Titel

Alzheimer's Disease and Advanced Drug Delivery Strategies

Auflage

First edition

Ort / Verlag

London, England : Academic Press,

Erscheinungsjahr

[2024]

Link zum Volltext

• Elsevier Books AutoHoldings

Beschreibungen/Notizen

• Includes index.
• Front Cover -- ALZHEIMER'S DISEASE AND ADVANCED DRUG DELIVERY STRATEGIES -- ALZHEIMER'S DISEASE AND ADVANCED DRUG DELIVERY STRATEGIES -- Copyright -- Contents -- Contributors -- About the editors -- Preface -- Acknowledgments -- 1 - Etiology, pathogenesis of Alzheimer's disease and amyloid beta hypothesis -- 1. Introduction -- 2. Etiology of Alzheimer's disease -- 3. Pathogenesis of Alzheimer's disease -- 3.1 Amyloid deposition neuropathogenesis -- 3.2 Neurofibrillary changes based neuropathogenesis -- 4. Diagnosis of AD -- 5. Amyloid beta protein hypothesis -- 6. Consequences of amyloid beta (Aβ) formation -- 7. Genetic factors responsible for the Alzheimer's disease -- References -- 2 - Neuroinflammation in Alzheimer's disease -- 1. Introduction -- 2. History of neuroinflammation in AD -- 3. The concept of neuroinflammation in AD -- 4. Neuroinflammation: Causes and consequences of Alzheimer's disease -- 5. BBB integrity and neuroinflammation -- 6. Role of cellular players -- 6.1 Microglial -- 6.2 Astroglia -- 6.3 Blood-derived mononuclear cells -- 7. Role of mediators and modulators in neuroinflammation -- 7.1 Cytokines -- 7.2 Interleukin-1 (IL-1) -- 7.3 Interleukin-6 (IL-6) -- 7.4 Tumor necrosis factor-alpha (TNF-α) -- 7.5 Transforming growth factor beta (TGF-β) -- 7.6 Chemokines -- 7.7 Caspases -- 7.8 Inflammatory changes of neurovascular unit (NVU) -- 7.9 Analysis of altering immune response -- 7.10 Nitric oxide and reactive oxygen species -- 7.11 Complement system -- 8. Role of intracellular signaling pathway -- 8.1 Role of MAPK -- 8.2 Role of NF-κB -- 8.3 Role of PPAR-γ -- 9. Genetic studies -- 10. Imaging of neuroinflammation in AD -- 10.1 The in-vivo laser scanning microscope -- 10.2 The imaging of inflammation in animals -- 10.3 The imaging of inflammation in humans -- 11. Possible intervention of neuroinflammation in AD.
• 11.1 Targeting inflammasome -- 11.2 Targeting CD38 -- 11.3 Targeting CD33 -- 11.4 Targeting TNF-alpha (TNF-α) -- 12. Factors associated with neuroinflammation -- 12.1 Traumatic brain injury (TBI) -- 12.2 Systemic inflammation -- 12.3 Obesity -- 12.4 Locus Coeruleus degeneration -- 13. Development of therapeutic potential -- 13.1 Antiinflammatory agents -- 13.2 Nutraceuticals -- 13.3 Essential vitamins and minerals -- 13.4 Antioxidants -- 14. Conclusion -- References -- 3 - Recent updates in chemistry of Alzheimer's: Synthetic molecules -- 1. Introduction -- 2. MTDL approach associated with following scaffold or structures -- 2.1 Acridine/tacrine analogs -- 2.2 Imidazoles and benzimidazoles -- 2.3 Coumarin and chromones -- 2.4 Donepezil analogs (indanone scaffold) -- 2.5 Indoles -- 2.6 Pyrazoles/pyrazolones -- 2.7 Triazoles -- 3. Conclusion -- References -- 4 - Blood brain barrier and its significance in drug delivery to brain in Alzheimer disease -- 1. Introduction -- 2. Blood brain barrier -- 3. Current treatments for AD -- 4. Emerging therapies for AD -- 5. Nanotherapeutics for AD -- 5.1 Polymeric nanoparticles -- 5.2 Lipidic-based systems -- 5.3 Metallic nanoparticles -- 5.4 Quantum dots -- 5.5 Dendrimers -- 5.6 RNA based systems -- 6. Other approaches for crossing BBB -- 6.1 Focused ultrasound (FUS) induced BBB opening -- 6.2 Implants -- 7. Conclusion and future perspective -- References -- 5 - Nose to brain delivery for the treatment of Alzheimer's disease -- 1. Introduction -- 2. The nose-to-brain (N2B) pathway -- 3. AZD and current treament -- 4. Development of N2B delivery for AZD -- 5. Approaches to modulation of N2B delivery in AZD -- 5.1 Solution -- 5.2 Mucoadhesive agents -- 5.3 Permeation enhancers -- 5.4 Colloidal carrier systems -- 5.4.1 Microemulsion -- 5.4.2 Nanoparticles -- 5.4.3 Nanosuspension -- 5.4.4 SLN and NLC.
• 5.4.5 Liposomes -- 6. Advantages of N2B delivery for AZD -- 7. Conclusion and future directions -- References -- 6 - Amyloid cascade hypothesis, tau synthesis, and role of oxidative stress in AD -- 1. Introduction to the amyloid (amyloid-beta peptide) -- 2. Biogenesis of amyloid-beta -- 3. Amyloid cascade hypothesis (ACH) -- 4. Pros and cons of the ACH -- 4.1 Pros -- 4.2 Cons -- 5. Therapeutic targeting for amyloid-beta in Alzheimer's pathogenesis -- 5.1 Inhibiting amyloid-beta production -- 5.1.1 Alpha-secretase activators -- 5.1.1.1 Etazolate -- 5.1.1.2 EGCG -- 5.1.1.3 Bryostatin 1 -- 5.1.2 Beta-secretase blockers -- 5.1.2.1 Thiazolidinedione analogs (rosiglitazone and pioglitazone) -- 5.1.2.2 CTS-21166 -- 5.1.2.3 MK-8931 -- 5.1.3 Gamma-secretase blockers -- 5.1.3.1 LY-450139 -- 5.1.3.2 GSI-953 -- 5.1.3.3 BMS-708163 -- 5.2 Blocking amyloid-beta aggregation -- 5.2.1 Tramiprosate -- 5.2.2 Curcumin -- 5.2.3 Resveratrol -- 5.2.4 Quercetins -- 5.2.5 Metal chelators -- 5.3 Increasing amyloid-beta clearance -- 5.3.1 Direct vaccination (amyloid-beta vaccination) -- 5.3.2 Passive immunization -- 5.3.2.1 Bapineuzumab -- 5.3.2.2 Solanezumab -- 5.3.2.3 Gantenerumab -- 5.3.2.4 Crenezumab -- 6. Tau protein -- 6.1 Pathophysiology of tau -- 6.1.1 Pathology of tau -- 6.1.1.1 Hyperphosphorylation and oligomerization of tau -- 6.1.1.2 Microtubule binding and redistribution -- 6.1.1.3 Formation of paired helical filaments (PHFs) -- 6.1.1.4 Modifications of tau -- 6.1.1.5 Glycation and truncation of tau -- 6.1.2 Physiological roles of tau -- 6.2 Tau-based therapies -- 6.2.1 Kinases inhibition -- 6.2.1.1 GSK3 inhibitors -- 6.2.1.2 CDK five inhibitors -- 6.2.1.3 MARK/PAR1 as a target for inhibition -- 6.2.2 Phosphatases activators -- 6.2.3 Microtubule stabilization -- 6.2.4 Glycosylation protagonist -- 6.2.5 Chaperones -- 6.2.6 Immunotherapy -- 6.2.7 Autophagic clearance.
• 7. Role of oxidative stress in AD -- 8. Corelation of amyloid B protein, tau process, and oxidative stress in AD -- References -- 7 - New biologicals and biomaterials in the therapy of Alzheimer's disease -- 1. Introduction -- 1.1 Alzheimer's pathophysiology -- 2. Potential target for Alzheimer's disease therapy -- 2.1 Targets associated with amyloid-beta (Aβ) protein -- 2.2 Targets associated with tau-protein -- 2.3 Targets associated with low levels of acetylcholine (ACh) -- 2.4 Genetic factors associated with Alzheimer -- 2.5 Role of dopamine and serotonin -- 2.6 Other potential targets -- 2.7 All FDA-approved therapies and modern research in the Alzheimer's disease -- 3. Biologicals used in therapy of Alzheimer's disease -- 3.1 Amyloid-beta therapeutic antibodies for AD -- 3.2 Tau therapeutic antibodies for AD -- 3.3 TREM2 therapeutic antibodies for AD -- 3.4 Neurotrophins for AD -- 3.5 TNF-α inhibitors for Alzheimer -- 3.6 Cell-based therapy -- 4. Biomaterials used in therapy of Alzheimer's disease -- 4.1 Implant-based drug delivery -- 4.1.1 Drug delivery and tissue engineering using implanted scaffolds -- 4.1.2 Injectable hydrogels for tissue engineering and drug delivery -- 4.2 Nanotechnology -- 5. Nanoparticles in the therapy of Alzheimer's disease -- 5.1 Curcumin-loaded nanoparticles -- 5.2 NP-mediated chelation -- 5.3 Nanoparticles loaded with iron (Fe) chelators -- 5.4 Copper chelators-induced nanoparticles -- 6. Metal nanoparticles for Alzheimer's disease treatment -- 6.1 Nanoparticles filled with cerium -- 6.2 Gold (Au) nanoparticles -- 6.3 Nanoparticles of selenium -- 7. Other NPs -- 7.1 Poly(butyl) cyanoacrylate (PBCA) NPs -- 7.2 Polymer-based NPs -- 7.3 Nano-particulates based on polysaccharides -- 7.4 Protein based nanoparticles -- 7.4.1 Functionalized synthetic polymers nanoparticles -- 7.5 NPs loaded with hormones.
• 7.5.1 Melatonin loaded nanoparticles -- 7.6 Self-assembling nanostructures -- 7.7 Self-assembling nanogel -- 7.8 Poly(propylene imine) dendrimers -- 7.9 Nanoparticles decorated with antibody or its fragment -- 7.10 Exosomes like nano-vesicular carriers -- 8. Systems based on biomaterials for mass production of therapeutic cells -- 8.1 Therapeutic cell isolation and purification -- 8.2 Genomic modification of therapeutic cells -- 8.3 Mass production of therapeutic cells -- 8.4 Harvesting cells after mass production -- 8.5 Cryopreservation, banking, and shipping -- 9. Challenges of biomaterial-based drug delivery approach in Alzheimer's disease -- 10. Conclusion -- References -- 8 - Roles of nano medicine in diagnosis of Alzheimer's disease -- 1. Introduction -- 1.1 Alzheimer's disease diagnostic and therapeutic pipelines: Current state -- 1.2 Clinical criteria for diagnosis -- 1.3 Pathogenesis of AD concerning diagnosis -- 2. Diagnostic tools for AD -- 2.1 History of diagnosis of AD -- 2.2 How is Alzheimer's disease diagnosed? [31] -- 2.2.1 Brain-imaging technologies used in diagnosis of AD [31,32] -- 2.2.2 Biomarkers -- 2.2.2.1 Diagnostic markers -- 2.2.2.2 Blood and fluid biomarkers -- 2.2.2.3 Ocular markers -- 2.2.2.4 Others -- 2.2.3 Optical imaging (OI) -- 2.2.4 Localized nanosensor based on surface plasmon resonance -- 2.2.5 Scanning tunneling microscopy [STM] and two photon Rayleigh spectroscopy -- 2.3 Nanotechnology for diagnosis of AD -- 2.3.1 Nano-diagnostics for AD -- 2.3.2 Nanotechnologies to detect AD biomarkers in biological fluids -- 2.4 Nano particles or nano medicine as a tool for diagnosis of AD -- 2.5 Need of nanomedicine as diagnostic approach -- 2.6 Preclinical and clinical tools for diagnosis of AD with marketed formulations available for diagnosis -- 3. Future perspective of nano medicine and their effectiveness.
• 4. Conclusion and limitations.
• Description based on print version record.