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Neuron Function Modulation

GLP-1 agonists, Galanin, P5 /P35, Humanin, Colivelin and others

In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

Exendin-4, GLP-1 & Liragutide

Click to Expand

GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.

Li Y at el. J Alzheimers Dis. 2010;19(4):1205-19.

Click to Expand

The diabetes drug liraglutide prevents degenerative processes in a mouse model of Alzheimer's disease.

McClean PL at el. J Neurosci. 2011 Apr 27;31(17):6587-94.

See more at Exendin-4 and GLP

GLP-1 (Human, Rat, Mouse) Related Products

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Exendin-4 Related Products

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In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

Galanin

Click to Expand

Neuroprotective role for galanin in Alzheimer's disease.

Counts SE at el. EXS. 2010;102:143-62.

Click to Expand

Endogenous Galanin Protects Mouse Hippocampal Neurons Against Amyloid Toxicity in vitro via Activation of Galanin Receptor-2.

Elliott-Hunt CR at el. J. Alzheimers Dis. 2011 Apr 6.

See more at Galanin

Galanin Related Products

%Galanin%

In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

P5 peptide Inhibits CDK5/P25 and Tau hyperphosphorylation

Click to Expand

A 24 residue peptide (P5), derived from P35, the CDK5 neuronal activator, specifically inhibits CDK5/P25 hyperactivity and tau hyperphosphorylation.

Zheng YL at el. J.Biol. Chem. 2010 Oct 29;285(44):34202-12.

See more at P5/P35 peptide

P5 Related Products

%018-72%

In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

Humanin

Click to Expand

A humanin derivative reduces amyloid Beta accumulation and ameliorates memory deficit in triple transgenic mice.

Niikura T at el. PLoS One. 2011 Jan 17;6(1):e16259.

 

Colivelin — A femtomolar-acting Humanin derivative mediated neuroprotection against Alzheimer's disease

Click to Expand

Development of a femtomolar-acting Humanin derivative named Colivelin by attaching activity-dependent neurotrophic factor to its N terminus: characterization of Colivelin-mediated neuroprotection against Alzheimer's disease-relevant insults in vitro and in vivo

Chiba T, et al. J Neurosci. 2005 Nov 2;25(44):10252-61

Click to Expand

Activity-dependent neurotrophic factor-9 and NAP promote neurite outgrowth in rat hippocampal and cortical cultures

Smith-Swintosky VL et al. J Mol Neurosci. 2005;25(3):225-38

Related Products

%018-31%;%018-32%;%018-34%;%Humanin%

In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

Hemopressin

Click to Expand

Modulation of the endocannabinoid system: neuroprotection or neurotoxicity?

Fowler CJ at el. Exp Neurol. 2010 Jul;224(1):37-47. Epub 2010 Mar 29.

Click to Expand

The endocannabinoid system and Alzheimer's disease.

Benito C at el. Mol Neurobiol. 2007 Aug;36(1):75-81. Epub 2007 Sep 5.

See more at Hemopressin

Hemopressin Related Products

%Hemopressin%

In addition to traditional therapies (such as passive immunotherapy, gamma-secretase inhibitors, IVIG - Passive/active vaccines, and Tau protein therapies), new approaches are emerging. These new approaches target correcting mitochondrial dysfunction or enhancing multi-level interactions (such as between genes, proteins, organelles, cells, organs, whole organism and environment) to correct molecular changes associated with Alzheimer´s disease.

It has been proposed that insufficiency of an endogenous defense system contributes to the disease progression of Alzheimer´s disease. Several endogenous factors play an important role in the neuroprotective and cognitive enhancement and reduce dystrophic neurite formation:

•Exendin-4, GLP-1 & Liragutide
•Galanin
•P5/P35 peptide
•Humanin
•Colivelin
•Hemopressin
•nAChR

nAChR

Click to Expand

Functional interactions of fibrillar and oligomeric amyloid-β with alpha7 nicotinic receptors in Alzheimer's disease.

Lilja AM at el. J Alzheimers Dis. 2011;23(2):335-47.

nAChR Related Products

%075-12%

alzheimer_home

%glp-%;%exe%;%galanin%;%18-72%,%018-31%;%018-32%;%018-34%;%humanin%;%hemopressin%;%075-12%


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