Gut mitochondrial defects drive neurodegeneration

With your good chance of getting dementia or Parkinsons, what is your doctor's EXACT PROTOCOL to fix those gut mitochondrial defects?

Your risks of dementia, has your doctor told you of this?

1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

2. Then this study came out and seems to have a range from 17-66%. December 2013.`    

3. A 20% chance in this research.   July 2013.

4. Dementia Risk Doubled in Patients Following Stroke September 2018

Where are the  protocols to prevent your dementia?

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017 

The latest here:

 

 

Gut mitochondrial defects drive neurodegeneration

• Ricardo Aparicio,
• Edward T. Schmid &
• David W. Walker 

Nature Aging volume 2, pages 277–279 (2022)Cite this article

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Neurodegenerative diseases, including Parkinson’s disease, are linked to the accumulation of defective mitochondria in the brain and to microbial dysbiosis in the gut. However, the interplay between these factors is incompletely understood. Fedele et al. reveal how gut mitochondrial dysfunction activates intestinal inflammation to drive neurodegeneration in a Parkinson’s disease model.

PD is an age-related neurodegenerative disease with symptoms ranging from mild tremors, speech disturbances and impaired writing ability to more severe manifestations such as slowed movements (bradykinesia), rigid muscles, impaired posture and balance, and loss of automatic movements. Over 10 million people worldwide have PD. As mitochondria accumulate damage with age, quality control mechanisms are essential to ensure homeostasis and maintain healthy cells and tissues. Dysfunctional mitochondria can be cleared and recycled via a specialized form of autophagy known as mitophagy. The gene PINK1 regulates mitophagy through recruitment of parkin to the outer membrane of depolarized mitochondria to tag it for degradation³. Mutations in the PINK1 gene have been linked to a form of familial PD and are associated with altered expression of metabolic and immune response genes³. Although hereditary mutations can affect cell physiology throughout the entire body, it seems reasonable to assume that impaired mitochondria in brain tissue has a prominent role in PD-related neurodegeneration. However, there are previously identified clues that suggest that alterations in the intestine could precede neurodegeneration in PD. For example, studies in patients with PD have shown that α-synuclein aggregates (which can contribute to PD) accumulate in peripheral nerves, including those that innervate the intestine⁴. These α-synuclein aggregates can propagate to the central nervous system, where they accumulate and cause neurotoxicity⁴. The primary question that the authors set out to address in this study² was whether mitochondrial dysfunction in brain tissue alone is responsible for PD-related neurodegeneration in the Pink1 Drosophila model of PD.

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