Journal of Neurochemistry

Cover image for Vol. 141 Issue 5

Edited By: Jörg Schulz

Impact Factor: 3.842

ISI Journal Citation Reports © Ranking: 2015: 71/256 (Neurosciences); 83/289 (Biochemistry & Molecular Biology)

Online ISSN: 1471-4159

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Recently Published Articles

  1. Sterol regulatory element binding protein-1C knockout mice show altered neuroactive steroid levels in sciatic nerve

    Nico Mitro, Gaia Cermenati, Matteo Audano, Silvia Giatti, Marzia Pesaresi, Silvia Pedretti, Roberto Spezzano, Donatella Caruso and Roberto Cosimo Melcangi

    Version of Record online: 29 MAY 2017 | DOI: 10.1111/jnc.14063

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    Mice lacking the lipogenic factor SREBP-1c develop peripheral neuropathy over time. We here illustrated the detected changes of neuroactive steroids in SREBP-1c knock-out sciatic nerve. At 2 months of age (mild neuropathy), mitochondria increase pregnenolone levels that is utilized for testosterone and estradiol production. At 10 months of age (severe neuropathy), mitochondria appear dysfunctional leading to increased synthesis of progesterone metabolites.

  2. Cross-sectional associations of cortical β-amyloid with erythrocyte membrane long-chain polyunsaturated fatty acids in older adults with subjective memory complaints

    Claudie Hooper, Philipe De Souto Barreto, Pierre Payoux, Anne Sophie Salabert, Sophie Guyonnet, Sandrine Andrieu, Bruno Vellas and for the MAPT/DSA study group

    Version of Record online: 29 MAY 2017 | DOI: 10.1111/jnc.14062

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    Polyunsaturated fatty acids (PUFAs) have been associated with reduced cognitive decline in observational studies. Hence, we examined the cross-sectional associations between cortical β-amyloid (Aβ) and erythrocyte membrane PUFAs in 61 non-demented elderly individuals. Although not significant, our results suggest that higher levels of erythrocyte membrane arachidonic acid (ARA) and lower levels of linoleic acid (LNA) are associated with increased cortical Aβ load in older adults at risk of dementia. The association of Aβ with ARA appears to be specific to apolipoprotein E e4 non-carriers. Thus, particular fatty acid profiles might modulate Aβ deposition.

  3. Reduced Muscle Strength in Ether Lipid-Deficient Mice Is Accompanied by Altered Development and Function of the Neuromuscular Junction

    Fabian Dorninger, Ruth Herbst, Bojana Kravic, Bahar Z. Camurdanoglu, Igor Macinkovic, Gerhard Zeitler, Sonja Forss-Petter, Siegfried Strack, Muzamil Majid Khan, Hans R. Waterham, Rüdiger Rudolf, Said Hashemolhosseini and Johannes Berger

    Accepted manuscript online: 29 MAY 2017 01:05AM EST | DOI: 10.1111/jnc.14082

  4. You have free access to this content
    Is sporadic Alzheimer′s disease a developmental disorder?

    Thomas Arendt, Jens Stieler and Uwe Ueberham

    Version of Record online: 28 MAY 2017 | DOI: 10.1111/jnc.14036

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    Alzheimer′s disease (AD) is a neurodegenerative disorder of higher age that specifically occurs in human. Here, we summarize recent evidence, that the evolutionary and developmental dimensions of brain structure and function provide the key to our understanding of AD.

    This article is part of a series “Beyond Amyloid”.

  5. Haplodeficiency of Cathepsin D does not affect cerebral amyloidosis and autophagy in APP/PS1 transgenic mice

    Shaowu Cheng, Willayat Y. Wani, David A. Hottman, Angela Jeong, Dongfeng Cao, Kyle J. LeBlanc, Paul Saftig, Jianhua Zhang and Ling Li

    Version of Record online: 26 MAY 2017 | DOI: 10.1111/jnc.14048

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    Previous studies in vitro have suggested that cathepsin D (Cat D) may play an important role in β-amyloidosis and autophagy-related processes in the brain. Using a mouse model in which one allele of the Cat D gene was deleted, we found that Cat D haplodeficiency had no impact on the level and deposition of amyloid-β (Aβ) in the brain of APP/PS1 double transgenic mice, which co-overexpress amyloid-β precursor protein (APP) with the Swedish double mutation and presenilin 1 (PS1) with deletion of exon 9. We further showed that Cat D haplodeficiency did not affect APP processing, the levels of other Aβ-degrading proteases such as insulin degrading enzyme and neprilysin, the levels of autophagy-related proteins, or the markers of neuroinflammation. Our findings demonstrate that in wild-type mice, cathepsin D protein levels are either in excess or redundant with other factors in the brain, and at least one allele of Cat D gene is dispensable for cerebral β-amyloidosis and autophagy in APP/PS1 transgenic mice.

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