ReviewPossible Causes of Alzheimer's Disease: Amyloid Fragments, Free Radicals, and Calcium Homeostasis
References (141)
- et al.
Cortical distribution of neurofibrillary tangles in Alzheimer's disease matches the pattern of neurons that retain their capacity of plastic remodelling in the adult brain
Neuroscience
(1998) - et al.
Methodological variables in the assessment of beta amyloid neurotoxicity
Neurobiol. Aging
(1992) - et al.
NT-3 and BDNF protect CNS neurons against metabolic/excitotoxic insults
Brain Res.
(1994) - et al.
Excitotoxic action of NMDA agonists on nigrostriatal dopaminergic neurons: Modulation by inhibition of nitric oxide synthesis
Brain Res.
(1995) - et al.
β-Amyloid peptides enhance binding of the calcium mobilising second messengers inositol (1,4,5)trisphosphate and inositol(1,3,4,5)tetrakisphosphate to their receptor sites in rat cortical membranes
Neurosci. Lett.
(1995) - et al.
In vitro
Eur. J. Pharmacol.
(1997) - et al.
Intraventricular infusion of antibodies to amyloid-β-protein precursor impairs the acquisition of a passive avoidance response in the rat
Neurosci. Lett.
(1990) - et al.
The biology of Alzheimer's disease
Mech. Ageing Dev.
(1996) - et al.
Inflammatory mechanisms in Alzheimer's disease
Trends Pharmacol. Sci.
(1994) - et al.
Lack of Alzheimer pathology after β-amyloid protein injections in rat brain
Neurobiol. Aging
(1992)
Neurodegeneration mediated by glutamate and β-amyloid peptide: A comparison and possible interaction
Brain Res.
APP transgenesis: Approaches toward the development of animal models for Alzheimer disease neuropathology
Neurobiol. Aging
Beta amyloid is neurotoxic in hippocampal slice cultures
Neurobiol. Aging
Release of prostaglandins during memory consolidation in the chick
Eur. J. Pharmacol.
L-AP4 (lS
Behav. Brain Res.
Nitric oxide, the enigmatic neuronal messenger: Its role in synaptic plasticity
Trends Neurosci.
Age related CNS disorder and early death in transgenic FVB/N mice overexpressing Alzheimer amyloid precursor proteins
Neuron
Free radicals and superoxide dismutase in blood of patients with Alzheimer's disease and vascular dementia
J. Neurol. Sci.
Glutamate-stimulated secretion of amyloid precursor protein from cortical rat brain slices
Neurochem. Int.
Changes of p53 in the brains of patients with Alzheimer's disease
Biochem. Biophys. Res. Commun.
Cellular delivery of NGF does not alter the expression of beta-amyloid immunoreactivity in young or aged nonhuman primates
Exp. Neurol.
In vivo
Neurobiol. Aging
Cell death induced by β-amyloid 1–40 in MES 23.5 hybrid clone: The role of nitric oxide and NMDA-gated channel activation leading to apoptosis
Brain Res.
Beta-amyloid induces apoptosis in human-derived neurotypic SH-SY5Y cells
Brain Res.
Bar expression in mammalian neurons undergoing apoptosis, and in Alzheimer's disease hippocampus
Brain Res.
Nitric oxide: A downstream mediator of calcium toxicity in the ischemic cascade
Neurosci. Lett.
Basic FGF attenuates amyloid beta-peptide-induced oxidative stress, mitochondrial dysfunction, and impairment of Na++
Brain Res.
Oxidative stress hypothesis in Alzheimer's disease
Free Radical Biol. Med.
Amyloid precursor proteins protect neurons of transgenic mice against acute and chronic excitotoxic injuriesin vivo
Neuroscience
β-Amyloid precursor protein and Alzheimer's disease: The peptide plot thickens
Neurobiol. Aging
β-Amyloid precursor protein metabolites and loss of neuronal Ca2+
Trends Neurosci.
Calcium-destabilizing and neurodegenerative effects of aggregated β-amyloid peptide are attenuated by basic FGF
Brain Res.
Degenerative and protective signaling mechanisms in the neurofibrillary pathology of AD
Neurobiol. Aging
Neuroprotective signal transduction: Relevance to stroke
Neurosci. Biobehav. Rev.
Reversion of beta25–35-amyloid peptide-induced amnesia by NMDA receptor-associated glycine site agonists
Brain Res.
β-Amyloid peptidein vitro
Neurobiol. Aging
Clinical comparison of Alzheimer's disease in pedigrees with the codon 717 Val → Ile mutation in the amyloid precursor protein gene
Neurobiol. Aging
Role of neurotransmission in the regulation of amyloid β-protein precursor processing
Biochem. Pharmacol.
Neuroprotective effects of the antioxidant LY231617 and NO synthase inhibitors in global cerebral ischaemia
Brain Res.
Amyloid beta toxicity consists of a Ca2+2+
J. Neurochem.
Amyloid beta-peptide stimulates nitric oxide production in astrocytes through an NFκB-dependent mechanism
Proc. Natl. Acad. Sci. USA
The ability of amyloid beta-protein (1–40) to form Ca2+
Ann. N.Y Acad. Sci.
Role of cyclic GMP in the regulation of neuronal calcium and survival by secreted forms of β-amyloid precursor
J. Neurochem.
ApoE-4 and age at onset of Alzheimer's disease: The NIMH genetics initiative
Neurology
A synaptic model of memory: Long-term potentiation in the hippocampus
Nature
Alzheimer's disease: Transiently developing dendritic changes in pyramidal cells of sector CA1 of the Ammon's horn
Acta Neuropathol. (Berlin)
Neuropathological stageing of Alzheimer-related changes
Acta Neuropathol.
The roles of conformation and aggregation in toxicity of beta-amyloid peptide (1–40) characterized with congo red
Soc. Neurosci. Meeting New Orleans
Cholinergic agonists and interleukin 1 regulate processing and secretion of the Alzheimer β/A4 amyloid precursor protein
Proc. Natl. Acad. Sci. USA
Release of excess amyloid β protein from a mutant amyloid β protein precursor
Science
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2014, Neurobiology of AgingCitation Excerpt :The application of a general (non-subtype-specific) mGluR agonist to primary neuronal cultures and brain slices has been reported to yield soluble APP secretion, indicating that one or more mGluRs are linked to the α-secretase processing of APP (Lee et al., 1995). In addition, group I mGluR-linked PLC activity is downregulated in the cerebral cortex of patients with AD (Albasanz et al., 2005), and it has been demonstrated that group I mGluRs accelerate the processing of APP into non-amyloidogenic APPs (Holscher, 1998; Louzada et al., 2001). Therefore, reduced group I mGluRs activity may facilitate amyloidogenic APP processing, thus contributing to the formation and deposition of Aβ observed in the common form of AD.
The incretin analogue D-Ala<sup>2</sup>GIP reduces plaque load, astrogliosis and oxidative stress in an APP/PS1 mouse model of Alzheimer's disease
2013, NeuroscienceCitation Excerpt :It is thought that in these early stages of the disease, astrocytes and microglia play an important role in the clearance of plaques, and it has been shown that removing astrocytes in the early stages of the disease result in an increased plaque load (Katsouri et al., 2012). Once the chronic inflammation is established, however, the inflammation response becomes neurotoxic due to the production of free radicals and pro-inflammatory cytokines (Holscher, 1998; Vaz et al., 2011). The significant increase of GFAP staining from 6 to 12 and 19 months corresponds to the increase in plaque load.