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Japanese encephalitis vaccines first became available in the 1930s. [3] One of them was an inactivated mouse brain-derived vaccine (the Nakayama and/or Beijing-1 strain), made by BIKEN and marketed by Sanofi Pasteur as JE-VAX, until production ceased in 2005.
Sanofi's drug, a monoclonal antibody, was discovered by Regeneron Pharmaceuticals and is called alirocumab. [126] An FDA warning in March 2014, about possible cognitive adverse effects of PCSK9 inhibition threw the competition into disarray, as the FDA asked companies to include neurocognitive testing into their Phase III clinical trials. [127]
These ICV injections result in models for the sporadic Alzheimer's disease (sAD) form, rather than familial. A characteristic of sAD is an insulin-resistant brain state (IRBS). Streptozotocin is a beta-cytotoxic drug and by injecting it directly into the cerebral ventricles, the treated mice develop symptoms that align with sAD symptoms in humans.
This drug does not cause sexual dysfunction or weight gain like the SSRIs but has a higher incidence of nausea. Methylphenidate is a much more reliable example of an NDRI (the action that it displays on the DAT usually getting preferential treatment).
Sanofi quoted Houman Ashrafian, its head of research and development, as saying that it "represents an unprecedented breakthrough as a potential first-in-disease treatment option with clinically ...
However drawbacks to this exist as well. Once the drug is in the brain there is a point where it needs to be degraded to prevent overdose to the brain tissue. Also if the drug cannot pass back through the blood–brain barrier, it compounds the issues of dosage and intense monitoring would be required. For this to be effective there must be a ...
The higher the dosage and the longer the drug is taken, the greater the risk of experiencing unpleasant withdrawal symptoms. Benzodiazepine treatment should only be discontinued via a slow and gradual dose reduction regimen.
Amisulpride is approved and used at low doses in the treatment of dysthymia and major depressive disorder. [10] [20] [11] [21] [22] [23] Whereas typical doses used in schizophrenia block postsynaptic dopamine D 2-like receptors and reduce dopaminergic neurotransmission, low doses of amisulpride preferentially block presynaptic dopamine D 2 and D 3 autoreceptors and thereby disinhibit dopamine ...