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New cannabinoid product may help treat Alzheimer's disease
The following is essential a press release for a company (India Globalization Capital, Inc.) that has developed a new cannabis produce (Hyalolex). I don't know how successful it will be, but I think that they have correctly identify how their product targets the specific causes of Alzheimer's disease.
India Globalization Capital Inc’s (NYSE American: IGC) Hyalolex, a cannabinoid-based therapy that appears to act on many different hypotheses of disease modalities...
Alzheimer’s disease affects over five million people in the United States and has become the sixth leading cause of death. Last year, the disease and related dementias cost the country $260 billion and is projected to cost about $1.1 trillion by 2050. It is America’s most expensive disease. About 10% of people over 65 are diagnosed with Alzheimer’s, and almost 66% of Alzheimer’s patients are women. At the same time, 35% of caregivers report that their health has gotten worse due to their care responsibilities, adding even further to the costs associated with the disease.
While there are several drugs that treat Alzheimer’s disease, the quest to cure the illness has frustrated even the largest pharmaceutical companies. The consensus for the past 25 years has been that the disease is caused by the build-up of a sticky plaque called beta amyloid in the brain. Billions of dollars were subsequently spent developing drugs to clear beta amyloid, but all of them have failed at various stages of clinical trials...
[Some] researchers believe that over-reactive oxygen molecules are causing oxidative stress, which could lead to the build-up of beta amyloid plaque and other “symptoms” of the disease. [the process that leads to oxidative stress leads to amyloid oligomers and plaques--the oligomers in turn are one of dozens of factors that contribute to oxidative stress].
India Globalization Capital’s Hyalolex (IGC-AD1) has been shown to act on many of these different pathways in early research studies. In addition to modulating beta amyloid production and inhibiting aggregation, the compound appears to inhibit hyperphosphorylation of tau proteins, enhance mitochondrial function, and modulate several endpoints of AD. The compound is also non-toxic to neurons and doesn’t product a “high” feeling.
Using an immunoblotting technique, Dr. Chuanhai Cao demonstrated that IGC-AD1 inhibits beta amyloid aggregation in a dose-dependent manner by increasing monomer levels. This addresses the “amyloid hypothesis” that states that the aggregation of amyloids into toxic oligomers is a key pathogenic event in the onset of AD. These plaques could also trigger other pathological events, such as oxidative damage and inflammation [again amyloid oligomers are only one of dozens of factors that cause inflammation and oxidative stress in Alzheimer's disease].
The same technique of using immunoblotting showed that IGC-AD1 reduced the expression of an enzyme that enables phosphorylation by as much as 53% to 62%, which reverses some of the pathological effects of overexpressed APP and tau proteins. This addresses the “tau protein hypothesis” that states that tau protein phosphorylation is three to four times higher than a normal brain, which could be the underlying cause of AD [tau hyperphosphorylation intereferes with neurotransmissions, which is one of several features of Alzheimer's disease].
Finally, Dr. Cao showed that IGC-AD1 enhanced mitochondrial function by between 30% and 60%, which could address the “mitochondrial cascade hypothesis”. This hypothesis is based on the notion that mitochondrial dysfunction - which worsens with age naturally - could start a cascade that ultimately leads to the disease. Evidence has also shown that elevated beta amyloid levels contribute to these mitochondrial abnormalities.
Other than the evidence showing that Hyalolex may address the three disease etiological hypothesis as outlined above, Hyalolex at larger doses may reduce patient anxiety, patient aggression, sleep disorder and alleviate overall caregiver distress.
Scientists are getting close to understanding the underlying mechanisms behind Alzheimer's disease that goes beyond the misleading assertion that amyloid oligomers and plaques or hyperphosphorylated tau are the causes of the disease. Once a fuller and better understanding of Alzheimer's disease is arrived at, the chances of finding more effective treatments for Alzheimer's disease rise dramatically.
Me, too. This was once an active place, full of ideas, research findings, and spirited conversations. The forum title used to be Medications/treatments for Alzheimer's. Then one member complained that the discussions were not scientific enough and that the information being provided was of poor quality. So the forum title was changed to clinical trials. I am not sure if the old members just left over time or if old and new members decided they could only talk about clinical trials. Whatever the case, some very inventive minds left Alzconnected. Occasionally one or two will come back, but most are gone forever. On a personal level, this meant the vast amount of information and knowledge that I used to get from this site, largely dried up.
The old site can still be accessed through the archive function.