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takyon [soylentnews.org] writes:

Merck has ended a trial [reuters.com] for the experimental Alzheimer's treatment verubecestat [wikipedia.org], a BACE1 inhibitor, after it was found to be ineffective. Biogen has increased the sample size of a trial for aducanumab [wikipedia.org], worrying some investors [marketwatch.com]. The news comes after the failure of drugs such as solanezumab [soylentnews.org] and intepirdine [soylentnews.org] to treat Alzheimer's and dementia.

The FDA has proposed [fda.gov] new guidelines that would make it easier to treat Alzheimer's [reuters.com] by lowering the bar for clinical success:

In proposed new guidelines released on Thursday, the FDA appears open to trial goals that better match early patient populations, including people who have yet to display memory loss or functional impairment, such as the ability to wash or dress themselves or cook meals.

The draft guidelines suggest that improvement in biomarkers, such as amount of beta amyloid in the brain, a protein linked to the disease, may be an acceptable goal for deeming a drug successful in patients with no symptoms. FDA guidelines used in prior studies demanded that a drug demonstrate both cognitive and functional improvements.

A bipartisan group of Senators and Congressman have introduced [thehill.com] the Concentrating on High-Value Alzheimer's Needs to Get to an End (CHANGE) Act [senate.gov], which would also reduce regulatory barriers faced by clinical trials. The annual cost of Alzheimer's and dementia care in the U.S. is projected to rise to $1.1 trillion by 2050.

Meanwhile, a group of researchers has found that targeting BACE1 enzymes could remove existing amyloid plaques [sciencenews.org] (in mice):

Knocking back an enzyme swept mouse brains clean of protein globs that are a sign of Alzheimer's disease. Reducing the enzyme is known to keep these nerve-damaging plaques from forming. But the disappearance of existing plaques was unexpected [rupress.org] [open, DOI: 10.1084/jem.20171831] [DX [doi.org]], researchers report online February 14 in the Journal of Experimental Medicine.

The brains of mice engineered to develop Alzheimer's disease were riddled with these plaques, clumps of amyloid-beta protein fragments, by the time the animals were 10 months old. But the brains of 10-month-old Alzheimer's mice that had a severely reduced amount of an enzyme called BACE1 were essentially clear of new and old plaques.

An Alzheimer's treatment, donepezil [wikipedia.org], has been used to treat alcohol-related brain damage in mice [dukehealth.org].

Finally, a study of eight patients with cerebral amyloid angiopathy [wikipedia.org] (CAA), a brain bleeding condition, found that all eight had undergone brain surgery earlier in life, suggesting that insufficiently clean surgical instruments could spread amyloid proteins from one person to another and cause CAA [newscientist.com]:

None of these people have known gene variants that would raise the risk of developing CAA early. [Sebastian] Brandner's team says the most likely explanation is that amyloid proteins were seeded into their bodies during childhood brain surgery, from instruments previously used for surgeries on people with Alzheimer's disease. Creutzfeldt-Jakob Disease (CJD), a brain disease caused by prion proteins, is already known to have been spread in a similar way.

Evidence of amyloid-β cerebral amyloid angiopathy transmission through neurosurgery [springer.com] (open, DOI: 10.1007/s00401-018-1822-2) (DX [doi.org])

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