Nature Search

Transplanted adrenal chromaffin cells in rat brain reduce lesion-induced rotational behaviour

William J. Freed
John M. Morihisa
Richard Jed Wyatt
Research23 Jul 1981
Nature

Volume: 292, P: 351-352
Chloroquine diverts ACTH from a regulated to a constitutive secretory pathway in AtT-20 cells

Hsiao-Ping Moore
Barry Gumbiner
Regis B. Kelly
Research31 Mar 1983
Nature

Volume: 302, P: 434-436
Functional recovery in parkinsonian monkeys treated with GDNF

Don M. Gash
Zhiming Zhang
Greg A. Gerhard
Research21 Mar 1996
Nature

Volume: 380, P: 252-255
Defects in enteric innervation and kidney development in mice lacking GDNF

José G. Pichel
Liya Shen
Heiner Westphal
Research04 Jul 1996
Nature

Volume: 382, P: 73-76
Is GDNF beneficial in Parkinson disease?

Glial cell line-derived neurotrophic factor (GDNF) has proved efficacious in treatment of neurodegeneration in toxin-induced models of Parkinson disease (PD), but clinical trials have been equivocal. Do the results of a recent study—suggesting that GDNF is ineffective in an α-synuclein-overexpression PD model—exclude GDNF as a therapy for PD?

Barry J. Hoffer
Brandon K. Harvey
News & Views20 Sept 2011
Nature Reviews Neurology

Volume: 7, P: 600-602
Maternally transmitted mitochondrial DNA mutations can reduce lifespan

Jaime M. Ross
Giuseppe Coppotelli
Lars Olson
ResearchOpen Access09 Oct 2014
Scientific Reports

Volume: 4, P: 1-3
Germline mitochondrial DNA mutations aggravate ageing and can impair brain development

Mutations in mitochondrial DNA (mtDNA) accumulate at a higher rate than mutations in nuclear DNA, and although somatic mtDNA mutations are known to be involved in mammalian ageing, the role of germline mutations in this process is unclear: here germline-transmitted mtDNA mutations are shown to be associated with ageing and brain malformations, and maternally transmitted mtDNA mutations may thus influence both development and ageing.

Jaime M. Ross
James B. Stewart
Nils-Göran Larsson
Research21 Aug 2013
Nature

Volume: 501, P: 412-415
Exercise Ameliorates Motor Deficits and Improves Dopaminergic Functions in the Rat Hemi-Parkinson’s Model

Yuan-Hao Chen
Tung-Tai Kuo
Barry J. Hoffer
ResearchOpen Access05 Mar 2018
Scientific Reports

Volume: 8, P: 1-18
CCL5 promotion of bioenergy metabolism is crucial for hippocampal synapse complex and memory formation

In addition to neuroinflammatory functions, chemokine CCL5 shows strong neurotrophic properties. In this study, we found that CCL5 facilitates hippocampal glucoregulatory efficiency. CCL5 promotes aerobic glucose metabolism, mitochondrial ATP generation and purine synthesis, improving synaptic plasticity and enhancing memory and cognition functions.

Reni Ajoy
Yu-Chun Lo
Szu-Yi Chou
ResearchOpen Access30 Apr 2021
Molecular Psychiatry

Volume: 26, P: 6451-6468
Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson’s disease

Shuchun Chen
Seong-Jin Yu
Yun Wang
ResearchOpen Access16 Jul 2018
Scientific Reports

Volume: 8, P: 1-13
Author Correction: Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson’s disease

Shuchun Chen
Seong-Jin Yu
Yun Wang
Amendments and CorrectionsOpen Access12 Sept 2018
Scientific Reports

Volume: 8, P: 1
CCL5/RANTES contributes to hypothalamic insulin signaling for systemic insulin responsiveness through CCR5

Szu-Yi Chou
Reni Ajoy
Barry Hoffer
ResearchOpen Access29 Nov 2016
Scientific Reports

Volume: 6, P: 1-13
Inhibition of Drp1 mitochondrial translocation provides neural protection in dopaminergic system in a Parkinson’s disease model induced by MPTP

Emily Filichia
Barry Hoffer
Yu Luo
ResearchOpen Access13 Sept 2016
Scientific Reports

Volume: 6, P: 1-13
Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

Lital Rachmany
David Tweedie
Chaim G. Pick
ResearchOpen Access16 Jun 2017
Scientific Reports

Volume: 7, P: 1-13

Search

Transplanted adrenal chromaffin cells in rat brain reduce lesion-induced rotational behaviour

Chloroquine diverts ACTH from a regulated to a constitutive secretory pathway in AtT-20 cells

Functional recovery in parkinsonian monkeys treated with GDNF

Defects in enteric innervation and kidney development in mice lacking GDNF

Is GDNF beneficial in Parkinson disease?

Maternally transmitted mitochondrial DNA mutations can reduce lifespan

Germline mitochondrial DNA mutations aggravate ageing and can impair brain development

Exercise Ameliorates Motor Deficits and Improves Dopaminergic Functions in the Rat Hemi-Parkinson’s Model

CCL5 promotion of bioenergy metabolism is crucial for hippocampal synapse complex and memory formation

Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson’s disease

Author Correction: Post-treatment with PT302, a long-acting Exendin-4 sustained release formulation, reduces dopaminergic neurodegeneration in a 6-Hydroxydopamine rat model of Parkinson’s disease

CCL5/RANTES contributes to hypothalamic insulin signaling for systemic insulin responsiveness through CCR5

Inhibition of Drp1 mitochondrial translocation provides neural protection in dopaminergic system in a Parkinson’s disease model induced by MPTP

Exendin-4 attenuates blast traumatic brain injury induced cognitive impairments, losses of synaptophysin and in vitro TBI-induced hippocampal cellular degeneration

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