Dr. Weeks’ Comments: The real message not to miss here is the frank acknowledgement that all the Alzheimer’s drugs don’t work.
“As more disappointing results emerge from anti-amyloid drug trials in Alzheimer’s (AD), there is growing interest in novel treatment approaches for this condition.”
The following is understood by corporate medical doctors:
“All drugs approved by the US Food and Drug Administration (FDA) for the treatment of AD are symptomatic therapies that modulate neurotransmitters, either acetylcholine or glutamate. The standard medical treatment for AD includes cholinesterase inhibitors (ChEIs) and a partial N-methyl-D-aspartate (NMDA) antagonist.They do not treat the underlying cause of AD nor halt the rate of decline.
The following classes of psychotropic medications have been used to treat the secondary symptoms of AD, such as depression, agitation, aggression, hallucinations, delusions, and sleep disorders [5] :
- Antidepressants
- Anxiolytics
- Antiparkinsonian agents
- Beta-blockers
- Antiepileptic drugs
- Neuroleptics “
So don’t waste your money with prescription drugs which do nothing to change the course of the dementia. As for the secondary symptoms, bio-identical progesterone cream with hemp, celery and lavender seeds which lowers adrenalin (like a beta blocker) and anti-inflammatory seed drinks (which are organic and non-GMO) do more and do it safer than any prescription drugs.
But now we learn that inflammation of the gums “gingivitis” is a risk factor for Alzheimer’s which must be remedied.
Readers of Corrective Health News already knew that Alzheimer’s disease, like all mental illnesses and cognitive malfunctions including autism and anxiety, is amplified by inflammation.
Also note the closing remark in this article:
“Several factors likely determine why one individual with Pg gets AD while another with the pathogen does not. For instance, it may be that some individuals have better blood–brain barrier function or a better immune response.”
You can understand that to mean that people with more anti-inflammation protecting themselves who therefore have tighter blood barrier junctions also have less dementia and Alzheimer’s disease symptoms.
So the best treatment for this dreaded dementia remains drinking, but also brushing your teeth with, anti-inflammatory seed drinks because the omega-6 fatty acids allow for the penetration through the gum tissues, the xylitol kills gum bacteria strept mutansand the effect is to optimize the anti-inflammatory properties of the seed oils to protect your brain! Nothing else does this as well so… Eat the seeds. Drink the seeds. And now Brush your Teeth with the seeds!
Gum Disease Bacteria a Novel Treatment Target for Alzheimer’s?
by Pauline Anderson July 22, 2019 SOURCE
As more disappointing results emerge from anti-amyloid drug trials in Alzheimer’s disease(AD), there is growing interest in novel treatment approaches for this condition.
One such approach is based on the hypothesis that Porphyromonas gingivalis (Pg), the bacteria involved in periodontal disease, may cause AD. The biopharmaceutical company Cortexyme Inc is testing this theory with an investigational agent COR388, which targets gingipains, the toxic proteases released by Pg.
Early results show the drug is well tolerated and promising in terms of biomarker findings. Organizers hope that a phase 2/3 trial of the treatment now under way will provide definitive efficacy results.
“Our findings suggest that there’s hope for a new and very different approach to Alzheimer’s disease”, Michael Detke, MD, PhD, chief medical officer for Cortexyme, told Medscape Medical News.
The findings were presented here at the Alzheimer’s Association International Conference (AAIC) 2019.
Downstream Inflammation
The gingipain hypothesis assumes that Pg is a key etiologic agent in AD. The thinking is that the infection causes downstream inflammation and signs of AD such as tau tangles, and amyloid-beta.
Research has already found that people with periodontal disease are at higher risk for AD. Some studies have shown that gum disease precedes AD, which dispels the idea that the bacteria is an effect of AD rather than a cause, said Detke.
The most important causal data come from a mouse model of AD, he said. “Several studies show that if you put Pg in the mouth of a mouse, it causes all the signs of Alzheimer’s disease.”
Studies have also shown that most patients with AD have Pg present in the brain. In collaboration with other groups, Detke’s team compared brain bank samples of patients with AD and age-matched controls who did not have AD. They found that the AD patients were statistically significantly more likely to have been infected with Pg.
“Almost 100% of the samples from Alzheimer’s patients had Pg, and about one third or maybe 40% of the control brains had Pg,” Detke said.
It makes sense that some individuals without AD would have the infection, as the hallmark pathological signs of the disease appear about 20 years before clinical symptoms, said Detke.
Several factors likely determine why one individual with Pg gets AD while another with the pathogen does not. For instance, it may be that some individuals have better blood–brain barrier function or a better immune response.