Aging, Amyloid, and Alzheimer's Disease: A Perspective in Honor of Carl Cotman
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Summary
The so-called amyloid (or Aß) hypothesis of AD is well supported scientifically and predicts several specific targets for therapeutic intervention, some of which are now reaching the clinic, providing the final and most important test for this hypothetical mechanism of disease.
- Type
- review
- Published
- 2003-11-01
- Cited by
- 106
- References
- 65
- OpenAlex
- https://openalex.org/W3114575
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:19115973
Keywords
Neuropathology, Honor, Perspective (graphical), Neuroscience, Disease
References
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- Photoactivated γ-secretase inhibitors directed to the active site covalently label presenilin 1
- Two transmembrane aspartates in presenilin-1 required for presenilin endoproteolysis and γ-secretase activity
- Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease
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- Beta-amyloid deposition and other measures of neuropathology predict cognitive status in Alzheimer's disease.
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- Amyloid β-peptide is produced by cultured cells during normal metabolism
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- Inflammation and Alzheimer's disease pathogenesis.
- Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red.
- Cerebrovascular transport of Alzheimer's amyloid beta and apolipoproteins J and E: possible anti-amyloidogenic role of the blood-brain barrier.
- Physical basis of cognitive alterations in alzheimer's disease: Synapse loss is the major correlate of cognitive impairment
- Oligomerization of endogenous and synthetic amyloid beta-protein at nanomolar levels in cell culture and stabilization of monomer by Congo red.
- Water-soluble A(N-40, N-42) Oligomers in Normal and Alzheimer Disease Brains (*)
- Correlation between elevated levels of amyloid beta-peptide in the brain and cognitive decline.
- The oligomerization of amyloid beta-protein begins intracellularly in cells derived from human brain.
Cited by
- Impact of the matrix metalloproteinase MMP-3 on dementia.
- Aβ peptides as one of the crucial volume transmission signals in the trophic units and their interactions with homocysteine. Physiological implications and relevance for Alzheimer’s disease
- Cyclopamine Modulates γ-Secretase-mediated Cleavage of Amyloid Precursor Protein by Altering Its Subcellular Trafficking and Lysosomal Degradation*
- The role of the C-terminal extension of αB-crystallin upon structure and function and the relationship with disease
- Interruption of [beta]-Catenin Signaling Reduces Neurogenesis in Alzheimer's Disease Brains
- Aβ1-16 Can Aggregate and Induce the Production of Reactive Oxygen Species, Nitric Oxide, and Inflammatory Cytokines
- Etude du mécanisme d’agrégation de la protéine Tau et son inhibition par des composés polyphénoliques
- Etude des effets des peptides amyloïdes : du fonctionnement de la synapse aux modifications du cytosquelette dans l'apoptose neuronale.
- Predicting cognitive impairment in Parkinson's disease using neurophysiology and biochemical parameters as biomarkers
- Statistical analysis for longitudinal MR imaging of dementia
- Clearance systems in the brain—implications for Alzheimer disease
- Modeling Sporadic Alzheimer's Disease: The Insulin Resistant Brain State Generates Multiple Long-Term Morphobiological Abnormalities Including Hyperphosphorylated Tau Protein and Amyloid-β
- Tissue Transglutaminase and Its Product Isopeptide Are Increased in Alzheimer's Disease and APPswe/PS1dE9 Double Transgenic Mice Brains
- Pathogenic Considerations in Sporadic Inclusion-Body Myositis, a Degenerative Muscle Disease Associated With Aging and Abnormalities of Myoproteostasis
- The anti-amnesic effects of luteolin against amyloid beta(25-35) peptide-induced toxicity in mice involve the protection of neurovascular unit.
- Behavioural phenotype of APPC100.V717F transgenic mice over-expressing a mutant Abeta-bearing fragment is associated with reduced NMDA receptor density.
- DHA-PC and PSD-95 decrease after loss of synaptophysin and before neuronal loss in patients with Alzheimer's disease
- Basal Forebrain Cholinergic Dysfunction in Alzheimer’s Disease – Interrelationship with β-amyloid, Inflammation and Neurotrophin Signaling
- Neuronal protection by bioactive nutrients.
- Intraneuronal tau aggregation precedes diffuse plaque deposition, but amyloid-β changes occur before increases of tau in cerebrospinal fluid
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