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originally posted by: seasonal
originally posted by: Gothmog
The problem I had with this was the 11 year old part...Unless I miss my guess , that is a lot old for beef cattle.
Usually MCdon's or another huge restaurant chain buys anything standing to grind.
originally posted by: M4ngo
Mad cow disease = prions
Cannabinoids protect you from getting neurodegenerative disease in the first place. Including, from prions, like in MCD.
Our results suggest that CBD may protect neurons against the multiple molecular and cellular factors involved in the different steps of the neurodegenerative process, which takes place during prion infection. When combined with its ability to target the brain and its lack of toxic side effects, CBD may represent a promising new anti-prion drug.
Nonpsychoactive Cannabidiol Prevents Prion Accumulation and Protects Neurons against Prion Toxicity
In the brains of CBD-treated mice, PrPres was barely detectable, whereas substantial amounts of PrPres were present in the brain of presymptomatic untreated control mice (Fig. 2A, top).
To determine whether CBD could affect prion disease in vivo, we infected wild-type mice (Fig. 1 D) by intraperitoneal inoculation with a high dose of 139A murine scrapie strain. This strain was chosen because its incubation period after peripheral inoculation is shorter and less variable than other strains (Carp et al., 1997). Starting on the day of infection (0 dpi) and continuing three times per week over a 4 week period, mice were treated with 20 mg/kg CBD. Treatment with CBD significantly increased the survival time of the infected wild-type mice compared with the vehicle-treated group ( p 0.02, Mann–Whitney test). Treatment over a longer period of time (up to 12 weeks) or treatment with a higher dose of CBD (60 mg/kg over 4 weeks) also led to a significant increase in the survival time of infected mice ( p 0.003 and 0.0003, respectively). To determine whether CBD also inhibited prion disease progression during the later stages of infection, we began treatment of infected mice at either 30 or 120 dpi. When 20 mg/kg CBD treatment was initiated at 30 dpi, the survival time of mice was significantly increased compared with the vehicle-treated group ( p 0.03). However, no significant difference was observed when CBD treatment was started at 120 dpi (data not shown). Overall, CBD delayed prion disease onset in scrapie-infected mice in a time- and concentration-dependent manner.
When treatment was applied starting the day of infection, CBD significantly delayed both the appearance of clinical signs of the disease (delay, 5.7 d; p 0.021) and death (delay, 5.4 d; p 0.022) compared with the vehicle-treated group. When CBD treatment started at 30 dpi (approximately one-third of the incubation time), no significant delay in the progression of the disease was observed. During the time course of these experiments, no significant side effects were seen in noninfected, CBD-treated mice (data not shown). In summary, our data demonstrate that, when applied the day of infection or as late as 1 month after infection, CBD slows down PrPres accumulation in the brains of prion-infected mice and delays the onset of terminal prion disease.
The addition of CBD appeared to decrease PrPres-induced neurotoxicity because the number and morphology of the neurons was similar to that observed in cells exposed to hgtsc (Fig. 5A). Neuronal viability was also monitored by mea- suring the reduction in mitochondrial activity using the MTS assay. CBD treatment resulted in a concentration-dependent in- crease in the number of viable neurons for both concentrations of hgtsc tested (Fig. 5B).
Because CBD has been shown to regulate microglia migration (Walter et al., 2003), it was of interest to determine whether or not CBD could affect this PrPres-induced chemotactic mechanism. The migration of N11 microglia toward a chamber containing neurons incubated with PBS, hgtsc or hgtsc was monitored in the presence of increasing concentrations of CBD (Fig. 5C). Hgtsc -exposed neurons induced an increase in the number of migrating microglia compared with hgtsc and PBS- exposed neurons. Importantly, no effect on the basal migration rate of microglial cells was observed with CBD alone, indicating that CBD by itself does not have in vitro chemotactic properties (Fig. 5C). Thus, CBD was able to impair PrPres-induced microglial cell migration in a concentration-dependent manner.
Here, we demonstrate that CBD increases the survival time of scrapie-infected mice, most likely by preventing cerebral accumulation of PrPres. Given that CBD inhibited PrPres accumulation in cells infected with both murine and sheep scrapie strains, it is likely that it will be effective against different TSE agents in different species.
Unexpectedly, we demonstrated that CBD does not inhibit PrPres formation in a cell-free assay in which the primary components are PrPsen and PrPres. It is therefore unlikely that CBD binds PrP isoforms. Rather, CBD may exert its anti-prion properties indirectly via more complicated cellular mechanisms that may be cell-type specific. The fact that inhibition of PrPres accumulation by CBD in scrapie-infected cells is slow, requiring passage of the cells several times in the presence of the drug to see an effect, is consistent with this idea.
Moreover, the idea of a mechanism of inhibition common to some cell types but not others is supported by the finding that CBD prevents PrPres formation in the brain, but not the spleen, of scrapie-infected mice. Alternatively, CBD may also hamper neuroinvasion from the periphery to the CNS. In this instance, because of its high lipophilicity, CBD could interact with neuronal cell membranes leading to membrane mod- ifications unfavorable to PrPres formation
Interestingly, it has recently been shown that cannabinoids prevent Alzheimer’s disease pathology via the blockade of microglial activation (Ramirez et al., 2005). Similarly, we demonstrated here that CBD protected neurons against PrPres toxicity and prevented PrPres-induced microglial cell migration. Thus, CBD may modulate glial cell function, leading to a reduction in the inflammatory response that usually accompanies neurodegeneration.
Together, our results suggest that CBD has the properties necessary to protect neurons against the multiple molecular and cellular factors involved in the different steps of the neurodegenerative processes that take place during TSE infection.
originally posted by: seasonal
... the sick animal was discovered during routine surveillance at an Alabama livestock market. The animal died at the market before entering the slaughter channels and samples were sent to a USDA lab in Iowa for confirmation.