Corrigendum to “The dark sides of amyloid in Alzheimer's disease pathogenesis” [FEBS Lett. 588 (5) (2014) 641–652]

Abstract

On page 642, paragraph 2, right column, line 12 the following reference should be inserted: [170]. Sorrentino, G. and Bonavita, V. (2007) Neurodegeneration and Alzheimer's disease: the lesson from tauopathies. Neurol. Sci. 28, 63-71.The first 19 lines of paragraph 4.2, on page 645, should read: ''APP seems to have a role in neural degeneration mostly as it is processed, rather than through Ab formation [15]. For instance, there is now broad evidence of the neuroprotective and neuroproliferative role of sAPPa in adult neuron [92,93]. Moreover, mice lacking APP show a smaller brain size [94], and sAPPa expression alone reverses this effect [95]. Furthermore, it has been showed that ERK-induced axon growth is prompted by sAPPa and sAPPb (generated in a 9:1 ratio) and that amino terminal fragments of APP can shift stem cell growth toward a neural phenotype [96]. Overall, all this evidence seems to suggest that APP processing might be an important inductor of neural stem cell differentiation [15] (Fig. 2).'' Lines 19-42, on page 646, paragraph 6.0, should read: ''The association between AD and ApoE is documented by observations of structural variants of the ApoE protein [133]. In humans, ApoE4 expression increases as a consequence of neuronal damage and a neuron-specific proteolysis, guided by astrocytes, takes place [151,152]. More specifically, ApoE4, cut by ApoE Cleaving Enzyme (AECE) and missing the 272-299 residues (D272-299), is not processed by the secretory pathway as it translocates to the cytosol [133]. On the other hand, D272-299-ApoE4 is integrated in the neurofibrillary tangle-like structures [152]. Accordingly, mice overexpressing cleaved-ApoE4 die within 4 months as they form AD-like neurofibrillary tangles. Furthermore, when mutated ApoE is expressed at lower levels, learning and memory deficits are observed at 6-7 months [153]. In addition, in Neuro-2a cell line, the D272-299-ApoE4 impairs complex III and IV respiratory functions [154], and mice expressing the same variant of ApoE display impaired axonal transport, with mitochondria accumulation in bulb-like dilations [133,155]. '' http://dx

Comparison between dynamic versus static models and real-time monitoring of neuronal dysfunction in an amyloid-β induced neuronal toxic model on a chip platform

“…It has been shown that the level of ACh receptors is reduced in AD and that cellular dysfunction and imbalance in neurotransmitter signaling could be responsible for the symptoms of AD. 36 Fig. 6(C) shows the quantification of ACh concentration after 5 days of culture with neural network formation in the static/ dynamic system and with/without 5 μM Aβ addition for 3 days.…”

Recent advances in molecular imaging probes for β-amyloid plaques

“…1,2 Although the precise mechanism leading to the development of AD has not been completely elucidated, the formation of Ab aggregates is widely accepted as the initial neurodegenerative event in AD brains. 3,4 Therefore, the in vivo detection of Ab plaques with molecular imaging techniques is expected to lead to the early diagnosis of AD and facilitate the discovery of effective therapeutic agents for it. 5,6 Molecular imaging techniques for the in vivo imaging of Ab plaques mainly include positron emission tomography (PET) and single photon emission computed tomography (SPECT) using radioactive probes, and optical imaging using uorescent probes.…”