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SCIENTIFIC SCORE
Possibly Effective
Based on 5 Researches
7.2
USERS' SCORE
Good
Based on 1 Review
8.5
Supplement Facts
Serving Size: 1 Softgel
Amount Per Serving
%DV
Zinc (from 150 mg Zinc Bisglycinate) (TRAACS™)
30 mg
273%
Pumpkin Seed Oil (Cold Pressed)
250 mg
†
Top Medical Research Studies
9
Zinc compound shows promise in Alzheimer
Carboxylated Zn-phthalocyanine attenuates brain Aβ in AD model mouse.
Strong link to Alzheimer's research
We explored how a carboxylated zinc compound, known as Zn-phthalocyanine (ZnPc), impacts Alzheimer’s disease by examining its effects on amyloid beta (Aβ) deposition in a specific mouse model. Over a 12-week period, we administered weekly injections of ZnPc to older J20 mice, carefully assessing their cognitive abilities through various behavioral tests. Early findings showed that this zinc-based treatment significantly improved learning and memory in these mice.
We found that ZnPc accumulated in the brain and effectively reduced levels of Aβ both within neurons and in surrounding areas. Notably, neuronal health appeared to improve as more neurons were observed in regions of the brain crucial for memory, like the cortex and hippocampus. The treatment also reduced harmful inflammatory responses, as indicated by fewer activated astrocytes and microglia, which are often involved in neurodegeneration.
Furthermore, improvements were noted in blood vessel integrity and overall brain structure, suggesting that ZnPc not only targets Aβ but also supports broader neurological health. In summary, our results propose that ZnPc may serve as a promising therapeutic agent for Alzheimer’s disease, emphasizing the potential of zinc and its compounds in addressing neurodegenerative issues.
We found that ZnPc accumulated in the brain and effectively reduced levels of Aβ both within neurons and in surrounding areas. Notably, neuronal health appeared to improve as more neurons were observed in regions of the brain crucial for memory, like the cortex and hippocampus. The treatment also reduced harmful inflammatory responses, as indicated by fewer activated astrocytes and microglia, which are often involved in neurodegeneration.
Furthermore, improvements were noted in blood vessel integrity and overall brain structure, suggesting that ZnPc not only targets Aβ but also supports broader neurological health. In summary, our results propose that ZnPc may serve as a promising therapeutic agent for Alzheimer’s disease, emphasizing the potential of zinc and its compounds in addressing neurodegenerative issues.
Read More
9
Zinc compound alters Aβ aggregation
A Cationic Zn-Phthalocyanine Turns Alzheimer's Amyloid β Aggregates into Non-Toxic Oligomers and Inhibits Neurotoxicity in Culture.
Investigates zinc's role in Alzheimer's
We set out to investigate the impact of a specific zinc compound, cationic methylated zinc-phthalocyanine (cZnPc), on the aggregation of amyloid β (Aβ) peptides, which are closely linked to Alzheimer’s disease. Previous research had shown that a different form of zinc-phthalocyanine could interact with Aβ, but it couldn’t pass through the blood-brain barrier. Thus, we were eager to see if cZnPc could influence this aggregation process and ultimately help address Aβ-related toxicity.
Through various tests, we discovered that cZnPc effectively inhibited Aβ fibril formation in a dose-dependent manner. Excitingly, instead of simply reducing the aggregation of Aβ, cZnPc promoted the formation of non-toxic oligomers early in the process, indicating a shift toward a less harmful state of the peptide. Our binding and simulation analyses showed that cZnPc interacts well with Aβ, enhancing the chances of these oligomers forming.
Importantly, in cell culture experiments, we found that cZnPc posed no toxicity, even at higher concentrations. Rather than being harmful, it actually protected neuronal cells from the damaging effects of Aβ. Overall, our findings suggest that cZnPc could be a promising avenue for Alzheimer’s therapy by altering the behavior of amyloid β and transforming it into a less dangerous form.
Through various tests, we discovered that cZnPc effectively inhibited Aβ fibril formation in a dose-dependent manner. Excitingly, instead of simply reducing the aggregation of Aβ, cZnPc promoted the formation of non-toxic oligomers early in the process, indicating a shift toward a less harmful state of the peptide. Our binding and simulation analyses showed that cZnPc interacts well with Aβ, enhancing the chances of these oligomers forming.
Importantly, in cell culture experiments, we found that cZnPc posed no toxicity, even at higher concentrations. Rather than being harmful, it actually protected neuronal cells from the damaging effects of Aβ. Overall, our findings suggest that cZnPc could be a promising avenue for Alzheimer’s therapy by altering the behavior of amyloid β and transforming it into a less dangerous form.
Read More
7
Zinc's potential in Alzheimer's treatment
Zinc homeostasis regulates caspase activity and inflammasome activation.
Relevant to Alzheimer’s treatment evaluation
We explored the potential role of zinc in treating Alzheimer’s disease through its effect on inflammasome activation, which is linked to inflammation and neurodegeneration. The study revealed that zinc ions (Zn2+) can inhibit the activity of caspase-1, an important player in the inflammasome pathway. By regulating this pathway, zinc helps to control inflammatory responses that could contribute to various diseases, including Alzheimer's.
Using a comprehensive approach, including genome-wide screening techniques, we identified SLC30A1, a zinc exporter, as a key regulator of inflammasome activity. Understanding how zinc and this zinc exporter interact provides insight into how zinc could be harnessed as a therapeutic option for conditions characterized by overactive inflammation.
Notably, zinc supplementation was shown to improve outcomes in sepsis, psoriasis, and Alzheimer's disease models. This suggests that boosting zinc levels might exert a protective effect by mitigating harmful inflammation. However, while the beneficial effects are promising, we acknowledge that further detailed research is essential to clarify the specifics of zinc’s role in Alzheimer's treatment.
Using a comprehensive approach, including genome-wide screening techniques, we identified SLC30A1, a zinc exporter, as a key regulator of inflammasome activity. Understanding how zinc and this zinc exporter interact provides insight into how zinc could be harnessed as a therapeutic option for conditions characterized by overactive inflammation.
Notably, zinc supplementation was shown to improve outcomes in sepsis, psoriasis, and Alzheimer's disease models. This suggests that boosting zinc levels might exert a protective effect by mitigating harmful inflammation. However, while the beneficial effects are promising, we acknowledge that further detailed research is essential to clarify the specifics of zinc’s role in Alzheimer's treatment.
Read More
Most Useful Reviews
8.8
Essential for Alzheimer
I regularly take this chelated zinc because the price is reasonable, and the quality is comparable to more expensive brands. This form is the most digestible. Zinc is vital for the nervous system's functioning, so it is important to take it with Parkinson's and Alzheimer.
Read More
Medical Researches
SCIENTIFIC SCORE
Possibly Effective
Based on 5 Researches
7.2
9
Zinc compound shows promise in Alzheimer
Carboxylated Zn-phthalocyanine attenuates brain Aβ in AD model mouse.
Strong link to Alzheimer's research
We explored how a carboxylated zinc compound, known as Zn-phthalocyanine (ZnPc), impacts Alzheimer’s disease by examining its effects on amyloid beta (Aβ) deposition in a specific mouse model. Over a 12-week period, we administered weekly injections of ZnPc to older J20 mice, carefully assessing their cognitive abilities through various behavioral tests. Early findings showed that this zinc-based treatment significantly improved learning and memory in these mice.
We found that ZnPc accumulated in the brain and effectively reduced levels of Aβ both within neurons and in surrounding areas. Notably, neuronal health appeared to improve as more neurons were observed in regions of the brain crucial for memory, like the cortex and hippocampus. The treatment also reduced harmful inflammatory responses, as indicated by fewer activated astrocytes and microglia, which are often involved in neurodegeneration.
Furthermore, improvements were noted in blood vessel integrity and overall brain structure, suggesting that ZnPc not only targets Aβ but also supports broader neurological health. In summary, our results propose that ZnPc may serve as a promising therapeutic agent for Alzheimer’s disease, emphasizing the potential of zinc and its compounds in addressing neurodegenerative issues.
We found that ZnPc accumulated in the brain and effectively reduced levels of Aβ both within neurons and in surrounding areas. Notably, neuronal health appeared to improve as more neurons were observed in regions of the brain crucial for memory, like the cortex and hippocampus. The treatment also reduced harmful inflammatory responses, as indicated by fewer activated astrocytes and microglia, which are often involved in neurodegeneration.
Furthermore, improvements were noted in blood vessel integrity and overall brain structure, suggesting that ZnPc not only targets Aβ but also supports broader neurological health. In summary, our results propose that ZnPc may serve as a promising therapeutic agent for Alzheimer’s disease, emphasizing the potential of zinc and its compounds in addressing neurodegenerative issues.
Read More
9
Zinc compound alters Aβ aggregation
A Cationic Zn-Phthalocyanine Turns Alzheimer's Amyloid β Aggregates into Non-Toxic Oligomers and Inhibits Neurotoxicity in Culture.
Investigates zinc's role in Alzheimer's
We set out to investigate the impact of a specific zinc compound, cationic methylated zinc-phthalocyanine (cZnPc), on the aggregation of amyloid β (Aβ) peptides, which are closely linked to Alzheimer’s disease. Previous research had shown that a different form of zinc-phthalocyanine could interact with Aβ, but it couldn’t pass through the blood-brain barrier. Thus, we were eager to see if cZnPc could influence this aggregation process and ultimately help address Aβ-related toxicity.
Through various tests, we discovered that cZnPc effectively inhibited Aβ fibril formation in a dose-dependent manner. Excitingly, instead of simply reducing the aggregation of Aβ, cZnPc promoted the formation of non-toxic oligomers early in the process, indicating a shift toward a less harmful state of the peptide. Our binding and simulation analyses showed that cZnPc interacts well with Aβ, enhancing the chances of these oligomers forming.
Importantly, in cell culture experiments, we found that cZnPc posed no toxicity, even at higher concentrations. Rather than being harmful, it actually protected neuronal cells from the damaging effects of Aβ. Overall, our findings suggest that cZnPc could be a promising avenue for Alzheimer’s therapy by altering the behavior of amyloid β and transforming it into a less dangerous form.
Through various tests, we discovered that cZnPc effectively inhibited Aβ fibril formation in a dose-dependent manner. Excitingly, instead of simply reducing the aggregation of Aβ, cZnPc promoted the formation of non-toxic oligomers early in the process, indicating a shift toward a less harmful state of the peptide. Our binding and simulation analyses showed that cZnPc interacts well with Aβ, enhancing the chances of these oligomers forming.
Importantly, in cell culture experiments, we found that cZnPc posed no toxicity, even at higher concentrations. Rather than being harmful, it actually protected neuronal cells from the damaging effects of Aβ. Overall, our findings suggest that cZnPc could be a promising avenue for Alzheimer’s therapy by altering the behavior of amyloid β and transforming it into a less dangerous form.
Read More
7
Zinc's potential in Alzheimer's treatment
Zinc homeostasis regulates caspase activity and inflammasome activation.
Relevant to Alzheimer’s treatment evaluation
We explored the potential role of zinc in treating Alzheimer’s disease through its effect on inflammasome activation, which is linked to inflammation and neurodegeneration. The study revealed that zinc ions (Zn2+) can inhibit the activity of caspase-1, an important player in the inflammasome pathway. By regulating this pathway, zinc helps to control inflammatory responses that could contribute to various diseases, including Alzheimer's.
Using a comprehensive approach, including genome-wide screening techniques, we identified SLC30A1, a zinc exporter, as a key regulator of inflammasome activity. Understanding how zinc and this zinc exporter interact provides insight into how zinc could be harnessed as a therapeutic option for conditions characterized by overactive inflammation.
Notably, zinc supplementation was shown to improve outcomes in sepsis, psoriasis, and Alzheimer's disease models. This suggests that boosting zinc levels might exert a protective effect by mitigating harmful inflammation. However, while the beneficial effects are promising, we acknowledge that further detailed research is essential to clarify the specifics of zinc’s role in Alzheimer's treatment.
Using a comprehensive approach, including genome-wide screening techniques, we identified SLC30A1, a zinc exporter, as a key regulator of inflammasome activity. Understanding how zinc and this zinc exporter interact provides insight into how zinc could be harnessed as a therapeutic option for conditions characterized by overactive inflammation.
Notably, zinc supplementation was shown to improve outcomes in sepsis, psoriasis, and Alzheimer's disease models. This suggests that boosting zinc levels might exert a protective effect by mitigating harmful inflammation. However, while the beneficial effects are promising, we acknowledge that further detailed research is essential to clarify the specifics of zinc’s role in Alzheimer's treatment.
Read More
7
Zinc's mixed efficacy in Alzheimer's
The Effect of Zeolite Zinc on Memory Performance and Hippocampal Cell Death in a Rat Model of Alzheimer's-like Disease Induced by Aβ.
Moderate relevance for Alzheimer's research
We explored the impact of zeolite zinc on memory and brain health in a rat model that simulates Alzheimer's disease. The study involved administering Aβ, a protein linked to Alzheimer's, to observe how zeolite zinc could improve memory performance and reduce brain cell death.
Using various tests like the Morris water maze and open field tests, we assessed spatial memory and anxiety-like behaviors in the rats. Our findings indicated that while zeolite zinc helped improve memory performance and reduced some negative effects associated with Aβ, it did not completely restore memory to baseline levels.
Furthermore, we noticed that Aβ increased the expression of certain proteins associated with Alzheimer's, as well as the number of dead cells in the brain. However, zeolite zinc appeared to lessen these harmful effects. This suggests that zinc has some beneficial properties in addressing Alzheimer's-like symptoms, but it also highlights the need for more research to determine the ideal dosing and potential combination therapies that might enhance its effectiveness.
Using various tests like the Morris water maze and open field tests, we assessed spatial memory and anxiety-like behaviors in the rats. Our findings indicated that while zeolite zinc helped improve memory performance and reduced some negative effects associated with Aβ, it did not completely restore memory to baseline levels.
Furthermore, we noticed that Aβ increased the expression of certain proteins associated with Alzheimer's, as well as the number of dead cells in the brain. However, zeolite zinc appeared to lessen these harmful effects. This suggests that zinc has some beneficial properties in addressing Alzheimer's-like symptoms, but it also highlights the need for more research to determine the ideal dosing and potential combination therapies that might enhance its effectiveness.
Read More
4
Zinc affects liver metabolism in Alzheimer’s
How does zinc chelation affect liver sphingolipid metabolism in an Alzheimer's-like model?
Combination treatment limits conclusions
We explored how zinc, when combined with Cyclo (His-Pro), impacts liver metabolism in a rat model of Alzheimer's disease. The study utilized an intracerebroventricular injection of amyloid beta-42 oligomers to mimic Alzheimer's symptoms in rats. Afterward, the rats received daily doses of the treatment for three weeks.
Our findings indicated that the administration of Cyclo-Z influenced the levels of various molecules associated with sphingolipid metabolism. Specifically, we observed increases in sphingosine 1 phosphate and glutathione while levels of ceramide and caspase-3 decreased. However, it’s interesting to note that Cyclo-Z treatment also led to higher levels of total oxidant capacity and 4-hydroxynonenal.
Ultimately, these results suggest that zinc could play a role in shifting liver metabolism toward a protective mode in the context of Alzheimer's. While our findings are promising, it’s essential to consider that Cyclo-Z was used in conjunction, which makes it challenging to isolate the effects of zinc alone.
Our findings indicated that the administration of Cyclo-Z influenced the levels of various molecules associated with sphingolipid metabolism. Specifically, we observed increases in sphingosine 1 phosphate and glutathione while levels of ceramide and caspase-3 decreased. However, it’s interesting to note that Cyclo-Z treatment also led to higher levels of total oxidant capacity and 4-hydroxynonenal.
Ultimately, these results suggest that zinc could play a role in shifting liver metabolism toward a protective mode in the context of Alzheimer's. While our findings are promising, it’s essential to consider that Cyclo-Z was used in conjunction, which makes it challenging to isolate the effects of zinc alone.
Read More
User Reviews
USERS' SCORE
Good
Based on 1 Review
8.5
8.8
Essential for Alzheimer
I regularly take this chelated zinc because the price is reasonable, and the quality is comparable to more expensive brands. This form is the most digestible. Zinc is vital for the nervous system's functioning, so it is important to take it with Parkinson's and Alzheimer.
