Genetically modified mosquitos and predatory bacteria could help us win the war against diseases carried by mosquitos and caused by superbugs. But hopes of an imminently available treatment for Alzheimer’s appear to have been dashed.

Just for once, the electorate voted yes. It was a vote in Monroe County, Florida, and no less than 57% of votes cast were in favour of the motion – the motion to release genetically modified mosquitos into an isolated region of the Florida Keys, in an attempt to wipe out the Zika virus in the area.

The company behind the big idea is the privately owned British firm Oxitec. It has developed technology to modify the DNA of male mosquitos, which will then be released into the wilds. The mosquitos then find young ladies to spend their time with, but the offspring of such unions, die before they reach maturity. So forget about killing off mosquitoes with pesticides, hit them where it hurts in the DNA. To say the idea is controversial in the Florida Keys area, which would be the test bed, is an understatement. “Genetically modifying mosquitoes and letting them into the wild to breed, what could possible go wrong?” they ask, somewhat ironically.

And while the Monroe County vote was positive, in Key Haven, the place where the release was due to take place, the majority voted against, so now authorities are looking for an alternative location.

But one advantage of this idea is that since the mosquitoes die off within a generation, one assumes that if something does go wrong, as critics fear, then within a mosquito generation things will go back to normal.

There is more than one way to skin of a mosquito, and much of the scientific world is watching CRISPR, a technology, that by the way uses techniques that are already applied by nature, to edit the DNA of mosquitoes such that they no longer carry such nasties as the Zika virus, or the big one, Malaria. But the innovation also involves something called a gene drive known as CAS9. A gene drive is technology that promotes the success of a particular gene, so that it is spread among the gene pool rapidly.

This is profound stuff, unlike the Florida experiment, the CRISPR techniques are much kinder to the mosquitos, it does not kill them off, rather it makes them less dangerous. On the other hand, if something does go wrong, unlike in the case of the Florida test, the mutation is here, forever.

That takes us to the another idea that scientists are playing with, this time to potentially win the war against superbugs – a war that has been going very badly of late. Few things are more important than this. The discovery of antibiotics has saved countless lives, if they lose their effectiveness, it would be like returning to pre-World War II medicine, a scratch could kill you. But now a team of scientists at Imperial College London and the University of Nottingham have been experimenting with Bdellovibrio bacteriovorus. Now this may not be a household name, but it could be rather important. It has been called killer bacteria. It feeds on other bacteria, and once it has finished feasting, it replicates and looks for other bacteria to tuck into.

For superbugs, Bdellovibrio bacteriovorus, is bad news. And forgive the schadenfreude among scientists, because no one seems to feel that sorry for the poor superbugs.

In trials, Bdellovibrio bacteriovorus, caused the population of the Shigella bacteria – a nasty superbug that makes 160 million people feel ill every year – to fall 4,000 fold. It’s early days, but

It’s early days, but technology to watch.

Sadly, solanezumab, a drug that was hailed as a potential treatment for Alzheimer’s, and being advanced by US pharmaceutical company Eli Lilly, has failed to live up to its previous promise. In tests, it was shown that the drug offered no significant advantage over a placebo. The company said “Lilly will not pursue regulatory submissions for solanezumab for the treatment of mild dementia due to Alzheimer’s disease.”

Alas, it turns out that between 2002 and 2012, 99.6% of drug studies concered with either preventing or curing the disease have been halted.

Then again, technology is advancing, ideas build on existing ideas, and computer modelling may eventually make it easier to develop new treatments. As recently as this month, reports circulated about a drug called verubecestat which, in tests involving monkeys and rats, was shown to reduce levels of amyloid beta in blood and spinal fluid, which has been associated with Alzheimer’s.

Other researchers for example from the University of New South Wales in Australia have been focusing on a specific protein, called tau, which may be linked to Alzheimer’s.

Just bear in mind, we only need to find a cure once, it matters not if 999 possible treatments fail, if we can find that one in a thousand.