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JournalISSN: 0895-8696

Journal of Molecular Neuroscience 

Springer Science+Business Media
About: Journal of Molecular Neuroscience is an academic journal published by Springer Science+Business Media. The journal publishes majorly in the area(s): Neuroprotection & Medicine. It has an ISSN identifier of 0895-8696. Over the lifetime, 4039 publications have been published receiving 101346 citations. The journal is also known as: JMN & Journal of molecular neuroscience MN.


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Journal ArticleDOI
TL;DR: While DTI offers a powerful tool to study and visualize white matter, it suffers from inherent artifacts and limitations and provides an efficient tool for comprehensive, noninvasive, functional anatomy mapping of the human brain.
Abstract: Diffusion tensor imaging (DTI) has become one of the most popular MRI techniques in brain research, as well as in clinical practice. The number of brain studies with DTI is growing steadily and, over the last decade, has produced more than 700 publications. Diffusion tensor imaging enables visualization and characterization of white matter fascicli in two and three dimensions. Since the introduction of this methodology in 1994, it has been used to study the white matter architecture and integrity of the normal and diseased brains (multiple sclerosis, stroke, aging, dementia, schizophrenia, etc.). Although it provided image contrast that was not available with routine MR techniques, unique information on white matter and 3D visualization of neuronal pathways, many questions were raised regarding the origin of the DTI signal. Diffusion tensor imaging is constantly validated, challenged, and developed in terms of acquisition scheme, image processing, analysis, and interpretation. While DTI offers a powerful tool to study and visualize white matter, it suffers from inherent artifacts and limitations. The partial volume effect and the inability of the model to cope with non-Gaussian diffusion are its two main drawbacks. Nevertheless, when combined with functional brain mapping, DTI provides an efficient tool for comprehensive, noninvasive, functional anatomy mapping of the human brain. This review summarizes the development of DTI in the last decade with respect to the specificity and utility of the technique in radiology and anatomy studies.

1,315 citations

PatentDOI
TL;DR: These findings establish the feasability of using nanotubes as substrates for nerve cell growth and as probes of neuronal function at the nanometer scale.
Abstract: A cell and substrate system and nerve regeneration implant are disclosed including a carbon nanotube and a neuron growing on the carbon nanotube. Both unfunctionalized carbon nanotubes and carbon nanotubes functionalized with a neuronal growth promoting agent may be utilized in the invention. A method is also disclosed for promoting neuronal growth.

674 citations

Journal ArticleDOI
TL;DR: It is concluded that widespread amyloid plaques in the neocortex best distinguishes very early stage AD, including “MCI” stage, and preclinical stages, from healthy brain aging and it is now critical to develop methods to detect preclinical AD during life.
Abstract: The results of studies from the Washington University Alzheimer Disease (AD) Research Center and those from other centers and investigators regarding the neuropathologic correlates of normal aging and early-stage AD are reviewed. We conclude that widespread amyloid plaques in the neocortex best distinguishes very early stage AD, including “MCI” stage, and preclinical stages, from healthy brain aging. Other AD lesions, including increased formation of neurofibrillary tangles and neuronal degeneration appear to result from the amyloid-initiated pathologic process, although they may have a more immediate effect on expression and severity of dementia. These data provide strong support for anti-amyloid intervention as a preventive therapy for AD. It is now critical to develop methods to detect preclinical AD during life.

498 citations

Journal ArticleDOI
TL;DR: The hypothesis that neuroactive steroids might represent a new therapeutic strategy for peripheral neuropathy is proposed.
Abstract: It is now well known that peripheral nerves are a target for the action of neuroactive steroids. This review summarizes observations obtained so far, indicating that through the interaction with classical and nonclassical steroid receptors, neuroactive steroids (e.g., progesterone, testosterone and their derivatives, estrogens, etc.) are able to influence several parameters of the peripheral nervous system, particularly its glial compartment (i.e., Schwann cells). Interestingly, some of these neuroactive steroids might be considered as promising neuroprotective agents. They are able to counteract neurodegenerative events of rat peripheral nerves occurring after experimental physical trauma, during the aging process, or in hereditary demyelinating diseases. On this basis, the hypothesis that neuroactive steroids might represent a new therapeutic strategy for peripheral neuropathy is proposed.

466 citations

Journal ArticleDOI
TL;DR: It is concluded that [Ser8]GLp-1 and the endogenous peptide GLP-1 can gain access to the brain from the periphery by simple diffusion and thus contribute to the regulation of feeding.
Abstract: Glucagon-like peptide-1 (GLP-1) reduces insulin requirement in diabetes mellitus and promotes satiety. GLP-1 in the periphery (outside the CNS) has been shown to act on the brain to reduce food ingestion. As GLP-1 is readily degraded in blood, we focused on the interactions of [Ser 8 ]GLP-1, an analog with similar biological effects and greater stability, with the blood-brain barrier (BBB). The influx of radiolabeled [Ser 8 ]GLP-1 into brain has several distinctive characteristics: 1. A rapid influx rate of 8.867 ± 0.798 × 10 4 mL/g-min as measured by multiple-time regression analysis after iv injection in mice. 2. Lack of self-inhibition by excess doses of the unlabeled [Ser 8 ]GLP-1 either iv or by in situ brain perfusion, indicating the absence of a saturable transport system at the BBB. 3. Lack of modulation by short-term fasting and some other ingestive peptides that may interact with GLP-1, including leptin, glucagon, insulin, neuropeptide Y, and melanin-concentrating hormone. 4. No inhibition of influx by the selective GLP-1 receptor antagonist exendin(9–39), suggesting that the GLP-1 receptor is not involved in the rapid entry into brain. Similarly, there was no efflux system for [Ser 8 ]GLP-1 to exit the brain other than following the reabsorption of cerebrospinal fluid (CSF). The fast influx was not associated with high lipid solubility. Upon reaching the brain compartment, substantial amounts of [Ser 8 ]GLP-1 entered the brain parenchyma, but a large proportion was loosely associated with the vasculature at the BBB. Finally, the influx rate of [Ser 8 ]GLP-1 was compared with that of GLP-1 in a blood-free brain perfusion system; radiolabeled GLP-1 had a more rapid influx than its analog and neither peptide showed the self-inhibition indicative of a saturable transport system. Therefore, we conclude that [Ser 8 ]GLP-1 and the endogenous peptide GLP-1 can gain access to the brain from the periphery by simple diffusion and thus contribute to the regulation of feeding.

440 citations

Performance
Metrics
No. of papers from the Journal in previous years
YearPapers
202342
2022171
2021291
2020227
2019200
2018188