Here some of them :
Modification of hippocampal excitability in brain slices pretreated with a low nanomolar concentration of Zn2.
Takeda A, Shakushi Y, Tamano H.
J Neurosci Res. 2015 Aug 13. doi: 10.1002/jnr.23629. [Epub ahead of print]
Select item 26204819
Influx of extracellular Zn(2+) into the hippocampal CA1 neurons is required for cognitive performance via long-term potentiation.
Takeda A, Suzuki M, Tempaku M, Ohashi K, Tamano H.
Neuroscience. 2015 Sep 24;304:209-16. doi: 10.1016/j.neuroscience.2015.07.042. Epub 2015 Jul 21.
Select item 26044210
Excess influx of Zn(2+) into dentate granule cells affects object recognition memory via attenuated LTP.
Suzuki M, Fujise Y, Tsuchiya Y, Tamano H, Takeda A.
Neurochem Int. 2015 Aug;87:60-5. doi: 10.1016/j.neuint.2015.05.006. Epub 2015 Jun 1.
Select item 25959547
Is interaction of amyloid β-peptides with metals involved in cognitive activity?
Tamano H, Takeda A.
Metallomics. 2015 Aug 5;7(8):1205-12. doi: 10.1039/c5mt00076a.
Select item 25818846
Regulation of extracellular Zn(2+) homeostasis in the hippocampus as a therapeutic target for Alzheimer's disease.
Takeda A, Tamano H.
Expert Opin Ther Targets. 2015 Aug;19(8):1051-8. doi: 10.1517/14728222.2015.1029454. Epub 2015 Mar 27.
Select item 25603776
Blockade of intracellular Zn(2+) signaling in the dentate gyrus erases recognition memory via impairment of maintained LTP.
Tamano H, Minamino T, Fujii H, Takada S, Nakamura M, Ando M, Takeda A.
Hippocampus. 2015 Aug;25(8):952-62. doi: 10.1002/hipo.22418. Epub 2015 Feb 11.
Worth reading this 2 months old free paper again and look at the other papers the authors recommend.
Front Aging Neurosci. 2015; 7: 116.
Published online 2015 Jun 17. doi: 10.3389/fnagi.2015.00116
Editorial: The molecular pathology of cognitive decline: focus on metals
So these are comming and there is nothing yet on the web page. How do you know that these are comming? Could you explain a bit more, please.
While waiting PBT434 studies, it good to read this, hope it is not posted earlier.
Metallomics. 2015 Jul 8;7(7):1091-102. doi: 10.1039/c4mt00345d.
Reactivity of copper-α-synuclein peptide complexes relevant to Parkinson's disease.
Dell'Acqua S1, Pirota V, Anzani C, Rocco MM, Nicolis S, Valensin D, Monzani E, Casella L.
Parkinson's disease (PD) is a neurodegenerative disorder characterized by the presence of abnormal α-synuclein (αSyn) deposits in the brain. Alterations in metal homeostasis and metal-induced oxidative stress may play a crucial role in the aggregation of αSyn and, consequently, in the pathogenesis of PD. We have therefore investigated the capability of copper-αSyn6 and copper-αSyn15 peptide complexes, with the 1-6 and 1-15 terminal fragments of the protein, to promote redox reactions that can be harmful to other cellular components. The pseudo-tyrosinase activity of copper-αSyn complexes against catecholic (di-tert-butylcatechol (DTBCH2), 4-methylcatechol (4-MC)) and phenolic (phenol) substrates is lower compared to that of free copper(ii). In particular, the rates (kcat) of DTBCH2 catalytic oxidation are 0.030 s(-1) and 0.009 s(-1) for the reaction promoted by free copper(ii) and [Cu(2+)-αSyn15], respectively. On the other hand, HPLC/ESI-MS analysis of solutions of αSyn15 incubated with copper(ii) and 4-MC showed that αSyn is competitively oxidized with remarkable formation of sulfoxide at Met1 and Met5 residues. Moreover, the sulfoxidation of methionine residues, which is related to the aggregation of αSyn, also occurs on peptides not directly bound to copper, indicating that external αSyn can also be oxidized by copper. Therefore, this study strengthens the hypothesis that copper plays an important role in oxidative damage of αSyn which is proposed to be strongly related to the etiology of PD.
This paper is already one month old and may be it was discussed here. It is a free paper and worth reading it again. Go and find it in pubmed.
Editorial: Metals and neurodegeneration: restoring the balance
Anthony R. White,1,* Katja M. Kanninen,2 and Peter J. Crouch1
This paper is not related to AD or HD, but could be one day related to Prana.
Chemotherapy (Los Angel). 2015 Jun;4(2). pii: 152.
Evidence that Human Prostate Cancer is a ZIP1-Deficient Malignancy that could be Effectively Treated with a Zinc Ionophore (Clioquinol) Approach.
Costello LC1, Franklin RB1, Zou J2, Naslund MJ3.
1Department of Oncology and Diagnostic Sciences; Dental School; and The Greenebaum Cancer Center; University of Maryland; Baltimore, USA.
2Department of Oncology and Diagnostic Sciences; Dental School; University of Maryland; Baltimore, USA.
3Division of Urology, University of Maryland School of Medicine; Baltimore, USA.
Despite decades of research, no efficacious chemotherapy exists for the treatment of prostate cancer. Malignant prostate zinc levels are markedly decreased in all cases of prostate cancer compared to normal/benign prostate. ZIP1 zinc transporter down regulation decreases zinc to prevent its cytotoxic effects. Thus, prostate cancer is a "ZIP1-deficient" malignancy. A zinc ionophore (e.g. Clioquinol) treatment to increase malignant zinc levels is a plausible treatment of prostate cancer. However, skepticism within the clinical/biomedical research community impedes significant progress leading to such a zinc treatment. This report reviews the clinical and experimental background, and presents new experimental data showing Clioquinol suppression of prostate malignancy; which provides strong support for a zinc ionophore treatment for prostate cancer. Evaluation of often-raised opposing issues is presented. These considerations lead to the conclusion that the compelling evidence dictates that a zinc-treatment approach for prostate cancer should be pursued with additional research leading to clinical trials.
eso, that has been my opinion for a long time. Orphan status and these facts are the most important issues IMO but it looks like something more is needed to get conditional approval.