2014
DOI: 10.1177/1073858414529828
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Do Astrocytes Collaborate with Neurons in Spreading the “Infectious” Aβ and Tau Drivers of Alzheimer’s Disease?

Abstract: Evidence has begun emerging for the "contagious" and destructive Aβ42 (amyloid-beta42) oligomers and phosphorylated Tau oligomers as drivers of sporadic Alzheimer's disease (AD), which advances along a pathway starting from the brainstem or entorhinal cortex and leading to cognition-related upper cerebral cortex regions. Seemingly, Aβ42 oligomers trigger the events generating the neurotoxic Tau oligomers, which may even by themselves spread the characteristic AD neuropathology. It has been assumed that only ne… Show more

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Cited by 70 publications
(96 citation statements)
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References 140 publications
(246 reference statements)
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“…These ranges from the most popular Aβ hypotheses, cholinergic, tau and inflammation hypotheses [19]. Degeneration of brain function is caused by a number of signals, one of which is the impairment of the synapsis by Aβ [20][21][22][23]. This is contrary to the most commonly used Aβ hypotheses, which did not recognise the complex mechanism in AD pathophysiology [23].…”
Section: Introductioncontrasting
confidence: 47%
“…These ranges from the most popular Aβ hypotheses, cholinergic, tau and inflammation hypotheses [19]. Degeneration of brain function is caused by a number of signals, one of which is the impairment of the synapsis by Aβ [20][21][22][23]. This is contrary to the most commonly used Aβ hypotheses, which did not recognise the complex mechanism in AD pathophysiology [23].…”
Section: Introductioncontrasting
confidence: 47%
“…As a consequence, Ab 128 peptides spontaneously aggregate into soluble oligomers and 129 coalesce to form fibrils insoluble beta-sheet conformation and are 130 eventually deposited in diffuse senile plaques [8]. Some recent 131 studies has shown that Ab42 oligomers are produced by 132 cooperative activities of both neurons and its associated astrocytes 133 [9]. It has been observed that Ab42 oligomers induce oxidative 134 damage, promote tau hyperphosphorylation, results in toxic 135 effects on synapses and mitochondria [6,7].…”
mentioning
confidence: 98%
“…Recent studies have also highlighted the role of Ab oligomers 120 in synaptic impairment, suggesting that these are primarily the 121 only one among several other signals that destroy the integrity of 122 brain functions [1,8,9,14]. And formations of amyloid plaques that 123 develop in the later age appear to be rather late event [9]. 124 According to the amyloid cascade hypothesis, the APP is 125 normally cleaved by a-secretase and aberrantly processed by b-and g-secretases ( Fig.…”
mentioning
confidence: 98%
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