Another infective agent implicated in neurodegenerative disease
Seeing a Neuroi never has a happy ending and not seeing a Neuro always makes me better
Brief summary: My first specific Neuro symptom was in 2008 (nystagmus). I had a rapid deterioration neurologically from 2011, culminating with severe disability in mid 2014. I couldn't get to see a Neuro because of long waiting times and this is how I found CPNi helpsite and started the antibioticsi - very successfully. The rapid downward spiral stopped immemdiately and I have been regaining health and function since. I've had to attend to Methylation and severe Heavy Metal toxicity, and have now done 63x5 day pulses of Tinidazole. EVentually when I was seen I had an MRI result which showed moderately advanced brain shinkage. I was never given a diagnosis or follow up.
Following a couple of emergency hospital admissions for super high blood pressure">i, I tested for heavy metals. My BP is now normal after 1 year of chelation and my Herxes no longer produce hypertension. I also notice less chilling, higher body temperature and the return of sweating. I asked to be referred to the Neuros for treatment of Heavy Metal poisoning, but was ridiculed. I treated myself. However, as a result of this referral I got another MRI and a Spect scan. I got the results of these tests last week - showing frontero-temporal neurodegeneration, a variant of Alzheimer's (called FTD dementiai). According to research I should be dead by now as there is no treatment.
On researching more I found that coconut oil often helped people energise their brains, so I tried that. Gee, it nearly killed me with massive herx and I had to stop for a while. I'm back on it in a lower dose. Further research (the article above in pubmed) shows that it kills off Candida and other fungi - not just in the gut, but in the brain too.
For those of you who are still keen on progressing with your own healing, never cease searching for more knowledge. This is making a difference to me.
"Neurodegenerative diseasesi constitute a heterogeneous group of disorders of the central nervous system (CNSi) that are characterised by a slow and irreversible loss of neuronal functions. The aetiology of primary neurodegenerative diseases, such as Alzheimer’s disease (AD), multiple sclerosis (MSi), Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS), remains largely unknown. A common feature of many neurodegenerative diseases is the presence of aggregates of misfolded proteins (intracellulari inclusions) in regions of the CNS that can serve as neuropathological hallmarks for disease diagnosis1<,2<. Depending on the particular disease, these insoluble fibrillar aggregates can vary in distribution and composition3<"