a(PUBCHEM:135316034)

Entity

Name

135316034

Namespace

PUBCHEM

Namespace Version

None

Pattern

^\d+$

The greatest FImax was observed with Protandim at 135-fold, followed by bardoxolone methyl at 67-fold, dimethyl fumarate at 55-fold, and sulforaphane at 21-fold PubMed:22020111

When compared contemporaneously in the AREc32-based assay, FImax observed was in the order Protandim > bardoxolone methyl > dimethyl fumarate > sulforaphane. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

While Protandim, bardoxolone methyl, BG-12, and sulforaphane all have been demonstrated to modify gene expression profiles by activation of Nrf2, they have not been compared side by side, in the same cell line, under identical conditions. PubMed:22020111

In our gene expression data, SIRT1 was induced 1.75-fold by Protandim (p = 0.015). PubMed:22020111

SLC7A11, induced 76-fold, encodes a cystine/glutamate antiporter responsible for maintaining extracellular glutamate in the brain, and for importing cystine necessary for glutathione synthesis (Albrecht et al., 2010). PubMed:22020111

AKR1B10, induced 72-fold, encodes aldo–keto reductase family 1 member B10 which efficiently detoxifies mutagenic and carcinogenic alpha, beta-unsaturated carbonyls such as 4-hydroxynonenal (Zhong et al., 2009). PubMed:22020111

PTGR1 (aka LTB4DH), induced 68-fold, encodes leukotriene B4-12-hydroxydehydrogenase, which is considered to be a key enzyme responsible for biological inactivation of prostaglandins and related eicosanoids (Tai et al., 2002). PubMed:22020111

HMOX1, induced 56-fold, encodes heme oxygenase-1, an antioxidant enzyme considered a hallmark of Nrf2 activation. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

AIFM2 (aka AMID), induced 29-fold, is implicated in caspase-independent apoptosis and was found to be downregulated in a majority of human tumors (Wu et al., 2004b). PubMed:22020111

OSGIN1 (aka OKL38), induced 29-fold, is an oxidative stress response gene and a tumor suppressor gene (Yao et al., 2008). PubMed:22020111

GPX3, induced 20-fold, encodes an important antioxidant enzyme, glutathione peroxidase-3, found normally in plasma and kidney but underexpressed in head and neck cancers (Chen et al., 2011). PubMed:22020111

SQSTM1, induced 20-fold, encodes sequestosome-1, a participant in the autophagy pathway recently shown to be necessary to avoid premature senescence in human fibroblasts (Kang et al., 2011). PubMed:22020111

HSPB8, induced 19-fold, is a heat shock protein that forms a complex with BAG3 (also induced 1.43-fold). PubMed:22020111

TNFSF9 (aka CD137L), induced 19-fold, can induce maturation of human immature monocyte-derived dendritic cells leading to an enhanced capacity of the dendritic cells to stimulate protective T cell responses, as compared to classical dendritic cells (Tang et al., 2011). PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

For example, 19 genes products have been associated with atherosclerosis and are up or down-regulated by Protandim. Of these 19 genes, the first 16 listed (84%) were regulated by Protandim in the opposing direction to that taken by the atherosclerosis disease process. The probable benefit of this effect of Protandim is further supported by the fact that of the 11 gene products currently being targeted by drug interventions (Table 1, in bold type), nine of them (Table 1, marked by asterisks) are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the therapeutic intervention. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In addition, Protandim downregulated the one gene targeted by a chemotherapeutic drug, an antimetabolite inhibitor for that gene’s product, thymidylate synthetase PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In colon carcinoma, IPA analysis revealed 28 genes associated with the disease that were also modulated by Protandim treatment. Of these, the first 25 listed (89%) were regulated by Protandim in the opposing direction to that taken by the colon carcinoma disease process. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

In Alzheimer disease, 66 genes were identified that are also modulated by Protandim at the gene expression level. Of these 66 genes, the first 43 of them (65%) were regulated by Protandim in the opposing direction to that taken by the Alzheimer disease process. The beneficial effect of Protandim is further supported by the fact that of the 10 gene products currently targeted by drug therapies, eight of them are modulated by Protandim in the same direction that is proposed to be beneficial and caused by the drug. PubMed:22020111

A likely explanation for the increased expression of GLRX2 (glutaredoxin 2) and NQO1 (NAD(P)H dehydrogenase, quinone 1) in colon carcinoma and of GLRX (glutaredoxin), HMOX1 (heme oxygenase-1), NQO1, and SOD1 (superoxide dismutase 1) in Alzheimer is that it represents an adaptive attempt to partially compensate for the increased level of oxidative stress associated with these diseases. These antioxidant genes are also upregulated by Protandim, which would provide additional antioxidant protection beyond that achieved by the ROS-dependent induction of these enzymes in the diseased tissues. PubMed:22020111