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Alzheimer’s disease is an inherent, natural part of human brain aging : an integrated perspective. In: Free Neuropathology. Jg.3. 8.7.2022
Inhalt
Index
Summary
1. Introduction
2. β-amyloid and Tau
2a. β-amyloid (Aβ)
2b. Tau
3. Familial AD (fAD; early-onset familial Alzheimer’s disease: EOFAD), and the β-amyloid cascade hypothesis
4. Sporadic AD (sAD; Late-onset Alzheimer disease: LOAD)
5. NFTs and SPs in non-human brain aging
6. Synapses
7. Neurotransmitters, neuromodulators, and related receptors
7a. Acetylcholine (Ach) and acetylcholine receptors (AChR)
7b. Glutamate and glutamate receptors (GluRs)
7c. γ-aminobutyric acid (GABA) and GABA receptors
7d. Serotonin and 5-hydroxytryptamine (5-HT) receptors
7e. Noradrenergic system
7f. Adenosine receptors
7g. Endocannabinoids and cannabinoid receptors (CBRs)
8. Trophic factors and receptors
9. Endoplasmic reticulum stress
10. Failure to remove debris: the ubiquitin-proteasome system (UPS) and autophagy in sAD
11. Granulovacuolar degeneration (GVD)
12. Glial alterations in aging and sAD
12a. Astrocytes
12b. Microglia
12c. Oligodendrocytes
13. The neurovascular system in AD
14. Purine and pyrimidine metabolism in sAD
15. Epigenetics in brain aging and sAD
15a. Histone modifications, DNA methylation, and hydroxymethylation
15b. Non-coding RNAs
16. Microorganisms and sAD
16a. Microorganisms in the brain and oral cavity
16b. Gut microbiota
17. Seeding and spreading of β-amyloid and tau
17a. Seeding β-amyloid
17b. Tau seeding
17c. Multiple seeding foci of β-amyloid and tau pathology; vulnerable and resistant populations to tau seeding in brain aging and sAD
18. Neuronal death
19. Neuronal connectivity networks in brain aging and sAD
20. Human brain aging and preclinical AD
21. Primary age-related tauopathy (PART), rapidly progressive sAD, and sAD resilience
21a. PART
21b. Rapidly progressive AD
21c. sAD resilience
22. Biochemical changes beyond tau and β-amyloid at the the first stages of NFT pathology
22a. Aberrant cell-cycle re-entry, and altered adult neurogenesis
22b. Brain lipids
22c. Lipid rafts and cell membranes
22d. Mitochondria
22e. Oxidative stress damage
22f. Inflammation
22g. Protein synthesis impairment
22h. Dysregulated protein phosphorylation
23. Concluding comments
Abbreviations
Funding
Acknowledgements
References