Journal of Neuroscience Research最新文献

Alzheimer's disease (AD) is a devastating form of dementia, with the number of affected individuals rising sharply. The main hallmarks of the disease include amyloid-beta plaque deposits and neurofibrillary tangles consisting of hyperphosphorylated tau protein, besides other pathological features that contribute to the disease's complexity. The causes of sporadic AD are multifactorial and mostly age-related and involve risk factors such as diabetes and cardiovascular or cerebrovascular disorders. Frontotemporal dementia (FTD) is another type of dementia characterized by a spectrum of behaviors, memory, and motor abnormalities and associated with abnormal depositions of protein aggregation, including tau protein. Currently approved medications are symptomatic, and no disease-modifying therapy is available to halt the disease progression. Therefore, the development of multi-targeted therapeutic approaches could hold promise for the treatment of AD and other neurodegenerative disorders, including tauopathies. In this article, we will discuss the pathophysiology of AD and FTD, the proposed hypotheses, and current therapeutic approaches, highlighting the development of novel drug candidates and the progress of clinical trials in this field of research.

Retinal ischemia is a significant pathological condition that contributes to visual impairment and neuronal cell death in various retinopathies. Evidence suggests that GABA release during ischemic events may exhibit neuroprotective properties, but conflicting findings highlight a potential shift in its effects due to altered chloride ion homeostasis. This study aimed to investigate the role of the GABAergic system in retinal ischemia, focusing on the temporal dynamics of GABA release and its impact on retinal damage. We hypothesized that ischemia-induced changes in GABA transport and chloride ion equilibrium contribute to neuronal damage, which can be mitigated by modulating GABAergic activity. Using an ex vivo chick retina model subjected to oxygen and glucose deprivation (OGD), during different times, we assessed morphological changes, cell death, GABA levels, transporter activity, and the levels of chloride cotransporters NKCC1 and KCC2. Pharmacological interventions, including picrotoxin and bumetanide, were used to evaluate neuroprotective effects. Our results revealed that OGD-induced significant morphological changes and cell death in the retina. GABA levels were reduced in a GAT-1-dependent manner, while picrotoxin and bumetanide demonstrated neuroprotective effects by mitigating retinal swelling and modulating the GABAergic system. Notably, OGD increased NKCC1 content, but not KCC2 levels, indicating a disruption in chloride homeostasis. These findings suggest that ischemia-induced alterations in GABAergic activity and chloride transport contribute to retinal damage. Targeting these pathways with pharmacological agents, such as bumetanide, may offer therapeutic strategies for mitigating ischemic retinal injury. Further research is recommended to explore the clinical applicability of these findings in the ischemic retina.

Although a cochlear implant (CI) can partially restore auditory function, CI recipients show alterations not only in auditory but also in visual cortical processing. Yet, it is not well understood how these visual changes relate to the CI outcome and to what extent these changes are induced by auditory deprivation and the limited CI input, respectively. Here, we present a prospective longitudinal electroencephalography study which examined the deprivation- and CI-induced alterations on cortical face processing by comparing visual evoked potentials (VEP) in CI users before and 6 months after implantation. A group of normal-hearing (NH) listeners served as a control. The participants performed a word-identification task and a face-categorization task to study the cortical processing of static and articulating faces in attended and unattended conditions. The CI candidates and CI users showed a reduced visual-cortex activation, a stronger functional connectivity between the visual and auditory cortex, and a reduced attention effect in the (extended) alpha frequency range (8–18 Hz) when compared to NH listeners. There was a positive correlation between the P1 VEP amplitude recorded before implantation and the speech recognition ability after implantation. Our results suggest that the CI users' alterations in cortical face processing are mainly induced by auditory deprivation and not by CI experience. Importantly, these deprivation-induced changes seem to be related to the CI outcome. Our results suggest that the visual P1 amplitude as recorded before implantation provides an objective index of cortical visual reorganization that may help predict the CI outcome.

Tubulin Polymerization Promoting Proteins (TPPPs) are highly conserved across species but remain poorly understood. There are three TPPP genes in humans, with only one homologous TPPP gene in invertebrates, such as Drosophila and C. elegans. The human TPPP (TPPP1/p25/p25α) is enriched in the brain and shares sequence similarities with the invertebrate TPPPs. TPPP/p25 associates with microtubules and plays a pivotal role in microtubule dynamics, bundling, and polymerization, thereby stabilizing the microtubular network. This is essential for cytoskeletal organization and proper functioning of neurons and glial cells, including axonal growth, regeneration, migration, trafficking, synapse formation, and myelination of axons. However, studies have also uncovered that besides its cytoplasmic/microtubular localization, TPPP/p25 is present in other subcellular compartments, including the mitochondria and nucleus, underscoring the presence of additional novel functions. At the molecular level, TPPP/p25 is predicted to exist as an intrinsically disordered protein and is implicated in neurological and neurodegenerative disorders, including Parkinson's and related disorders and Multiple Sclerosis. In this article, we provide a comprehensive overview of TPPP/p25, highlighting its evolutionary conservation, cellular and subcellular localization, established and emerging functions in the nervous system, interacting partners, potential clinical relevance to human neurological disorders, and conclude with unresolved questions and future areas of study.

EXPRESSION OF CONCERN: O. Ghribi, M. M. Herman and J. Savory, “Lithium Inhibits Aβ-Induced Stress in Endoplasmic Reticulum of Rabbit Hippocampus but Does Not Prevent Oxidative Damage and Tau Phosphorylation,” Journal of Neuroscience Research 71, no. 6 (2003): 853–862, https://doi.org/10.1002/jnr.10511.

This Expression of Concern is for the above article, published online on 04 February 2003 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and Wiley Periodicals LLC. The Expression of Concern has been agreed due to overlap between images presented in Figures 5H and 5I. Due to the time that has elapsed, the original raw data of this manuscript is no longer available. Although the conclusions are not believed to be affected, the journal is issuing this expression of concern to alert readers.

RETRACTION: A. Campisi, V. Bramanti, D. Caccamo, G. Li Volti, G. Cannavò, M. Currò, G. Raciti, F. Galvano, F. Amenta, A. Vanella, R. Ientile, R. Avola, “Effect of growth factors and steroids on transglutaminase activity and expression in primary astroglial cell cultures,” Journal of Neuroscience Research 86, no. 6 (2008): 1297–1305, https://doi.org/10.1002/jnr.21579.

The above article, published online on 26 November 2007 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley & Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 1 and 8 were duplicated and manipulated, and that portions of Figure 8 were duplicated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.

RETRACTION: V. Bramanti, S. Grasso, D. Tibullo, C. Giallongo, R. Pappa, MV Brundo, D. Tomassoni, M. Viola, F. Amenta, and R. Avola, “Neuroactive Molecules and Growth Factors Modulate Cytoskeletal Protein Expression During Astroglial Cell Proliferation and Differentiation in Culture,” Journal of Neuroscience Research 94, no. 1 (2016): 90-98, https://doi.org/10.1002/jnr.23678.

The above article, published online on 15 October 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley & Sons, Inc. Following publication, concerns were raised by a third party that portions of Figures 2B and 3 were duplicated and manipulated, and that most of the images from Figure 2A were duplicated and manipulated from an earlier publication by this research group. Internal investigation confirmed these claims. The publisher attempted to contact the authors and request original data, but the authors did not respond. The retraction has been agreed because of concerns that the images were manipulated, affecting the interpretation of the data and results presented. The authors have been notified of the retraction.

EXPRESSION OF CONCERN: A. Valerio, M. Ferrario, F.O. Martinez, M. Locati, V. Ghisi, L. Grazia Bresciani, A. Mantovani, P. Spano, “Gene Expression Profile Activated by the Chemokine CCL5/RANTES in Human Neuronal Cells,” Journal of Neuroscience Research 78, no. 3 (2004): 371-382, https://doi.org/10.1002/jnr.20250.

This Expression of Concern is for the above article, published online on 23 August 2004 in Wiley Online Library (wileyonlinelibrary.com), and has been issued by agreement between the journal Editor-in-Chief, Lawrence S. Sherman; and John Wiley & Sons, Inc. Following publication, concerns were raised by a third party that the control actin bands had been duplicated within Figure 2. While the image manipulation does not seem to affect the conclusions of the paper, the journal has decided to issue an Expression of Concern to inform and alert readers. The authors have been notified of the Expression of Concern.