Oxidative-stress - Schrag Laboratory https://schraglab.com Our mission​ - cure Cerebral Amyloid Angiopathy​ Sat, 07 May 2022 13:21:33 +0000 en-US hourly 1 https://wordpress.org/?v=6.6.2 https://i0.wp.com/schraglab.com/wp-content/uploads/2021/12/logo_symbol.png?fit=32%2C32&ssl=1 Oxidative-stress - Schrag Laboratory https://schraglab.com 32 32 201078762 Diet and Alzheimer’s https://schraglab.com/diet-and-alzheimers/?utm_source=rss&utm_medium=rss&utm_campaign=diet-and-alzheimers Tue, 21 Dec 2021 17:14:44 +0000 https://schraglab.com/?p=1096 One of the most complicated issues in clinical AD research is how diet contributes to cognitive decline.  There is also unfortunately a great deal of mythology in this area. As a scientist and physician, let me start by saying that we have no evidence that AD can be cured or slowed down by any dietary […]

The post Diet and Alzheimer’s appeared first on Schrag Laboratory.]]> One of the most complicated issues in clinical AD research is how diet contributes to cognitive decline.  There is also unfortunately a great deal of mythology in this area.

As a scientist and physician, let me start by saying that we have no evidence that AD can be cured or slowed down by any dietary intervention or dietary supplement at this time. 

There is no doubt, however, that diet plays a role in healthy aging and this is certainly as important for brain health as it is for heart health.  We have also discovered that a deficiency in non-enzymatic antioxidants in the blood (particularly vitamins A, C, E and carotenoids) is very common among patients with AD and this is likely due to dietary deficiencies.  While it is not yet proven that correcting these deficiencies slows or reverses AD, it is reasonable and appropriate clinically to encourage patients to eat a healthy diet, rich in fruits, vegetables and nuts with natural antioxidants.  It may also be reasonable to consider gentle supplementation to correct specific deficiencies in specific nutrients for individual patients. 

I am particularly wary of supplementing non-enzymatic antioxidants to non-physiologic levels, because this may cause unexpected consequences.  Vitamin E in particular at high doses can behave in a pro-oxidant fashion and may actually decrease total antioxidant capacity of the blood (see here, here and here).  There is at least one meta-analysis which has associated high-dose vitamin E supplementation with all-cause mortality.  For these reasons, I am reluctant to encourage high-doses of any dietary supplement for my patients outside of a clinical study.

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The post Diet and Alzheimer’s appeared first on Schrag Laboratory.]]> 1096 Oxidative stress in Alzheimer’s disease and CAA https://schraglab.com/oxidative-stress-in-alzheimers-disease-and-caa/?utm_source=rss&utm_medium=rss&utm_campaign=oxidative-stress-in-alzheimers-disease-and-caa Tue, 21 Dec 2021 17:10:43 +0000 https://schraglab.com/?p=1093 One major proposed mechanism to explain changes associated with cellular and organismal aging is that oxidative damage to lipid, protein and nucleic acids accumulates as cells become less capable of coping with oxidative stress.  This potentially leads to membrane instability, accumulation of damaged proteins and acquired mutation, all of which may contribute to cellular dysfunctions […]

The post Oxidative stress in Alzheimer’s disease and CAA appeared first on Schrag Laboratory.]]> One major proposed mechanism to explain changes associated with cellular and organismal aging is that oxidative damage to lipid, protein and nucleic acids accumulates as cells become less capable of coping with oxidative stress.  This potentially leads to membrane instability, accumulation of damaged proteins and acquired mutation, all of which may contribute to cellular dysfunctions associated with aging and aging related diseases.

The role of oxidative stress as it contributes to neuronal dysfunction in the context of aging and Alzheimer’s disease (AD) is of particular interest and has generated enormous observational and experimental literature. Despite this, large scale clinical trials of antioxidative therapy have not yet produced a compelling therapy for AD. Additionally, specific mechanisms which contribute to oxidative stress in the brain are not clear. The large volume of literature and heterogeneity of results makes a comprehensive understanding of the changes occurring in the human brain in Alzheimer’s disease elusive.

To address this, we are conducting analyses and meta-analyses to map the network of oxidative stress-related changes in the brain and blood in AD to try to better define the changes to determine if there is a broad dysregulation or a more-specific pattern to explain reported changes.

Oxidative stress in Alzheimer's disease and CAA
The diagram at the left describes some of the best-known oxidative stress related pathways to give a sense for how complex this system is. And changes in this network can occur in the serum, in circulating blood cells, in peripheral organs and in every cell type in the brain and each of these potentially interacts with all the others. This is why data from the oxidative stress arena can be so hard to interpret and why we have invested in analysis that looks at these variables as networks.

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