EACH month brings a new insight into BSE and CJD. It is a reflection of how little we know about these unusual diseases.
But despite the amount of research under way in Britain and elsewhere, and the breakthroughs made in the past year, there is much that we still do not know.
Consider the last 12 months. In October 1995 the main concern was the incidence of CJD among farmers.
Then in March came news of a new type of CJD. This variant (or vCJD) affected younger people but none of the 10 cases identified then was a farmer.
Was this a new disease? Was it caused by BSE? Or had the surveillance programme simply spotted something that would otherwise have been missed?
In July it emerged that some infected cows can pass the disease to their calves.
But it remains unclear how often this happens and, more importantly, how it happens. Is the disease transmitted via the placenta, blood or milk?
In August a team from Oxford predicted the end of BSE: the epidemic would be over by 2001, they said, even without culling.
But they also estimated the number of BSE cases in Britain so far to be 900,000. Since only 162,000 have been diagnosed, this means 730,000 infected animals have entered the food chain.
But are these estimates accurate? How many infected animals were eaten? And was offal from any of them eaten before the ban on offal was introduced in 1988?
Throughout all this, indeed for the last 10 years, there has been one major concern: can humans get BSE by eating contaminated beef and beef products?
Some pointed to scrapie, which has been around for centuries, and argued that if we could live with scrapie we could live with BSE.
In a wonderful piece of false logic, they may even have believed that if there was no evidence for BSE in humans, then that was evidence that there was no BSE in humans.
But there were also those who, even from the start, argued that at the very least it might be possible for humans to become infected. After all, BSE is different, even if it began as scrapie.
Moreover, we learned quite early that cats, antelope and many other species, but by no means all, could contract the disease by eating contaminated meat.
It has taken 10 years for the evidence to accumulate, but yesterday it emerged. The report, published in Nature by a team from Imperial College in London, vindicates those who said all along that humans were at risk.
Prof Richard Lacey, long a thorn in the side of British ministers, was right: people can get BSE, presumably by eating contaminated meat, and the new form of CJD might more accurately by called BSE in humans.
The new study is complex. The team devised a battery of biochemical tests that enabled them to profile or "fingerprint" the prion protein believed to be the root cause of these diseases. They then compared the fingerprints they observed for the various forms of CJD and BSE.
Their report contains three important findings. First, the new CJD is indeed different from the other known forms of the disease, its fingerprint is different.
But this fingerprint is the same as that seen for BSE, and not just BSE in cattle, but also BSE in cats, antelope and monkeys. The reasonable conclusion is that the new CJD is BSE in humans.
Finally, the other forms of CJD which they studied, and which account for most British cases, do not appear to be linked with BSE, as was the fear 12 months ago.
Oddly, the evidence of BSE in humans has not caused the shock one might have expected. Perhaps because it merely confirms what many have long suspected Perhaps because the beef crisis can get no worse.
But if the latest research answers old questions, it also highlights the mysteries that remain. Fourteen human cases of BSE have been identified but how many more can we expect? When did these people contract the disease? Was it before the 1988 ban on offal?
The British government says no further measures are needed following the findings. But it remains to be seen if there are any legal implications in yesterday's news for the families of those affected by the new form of CJD.
How consumers will react to the latest news will probably depend on their attitude to risk. You are more likely to contract the rare sporadic form of CJD (there are about 50 cases a year in the Britain) than to contract BSE.
Most importantly, the research highlights again the urgent need for a quick diagnostic test for BSE.
If one were available we might be able to ensure that all infected animals were kept out of the food chain.
The technique devised by the London team could form the basis for such a test but it would take years to turn their complex experimental methodology into a simple commercial test. By which time the BSE epidemic could have passed.
In the meantime, politicians and consumers want certainties. The picture has become clearer, many people's worst fears have now been realised.
But there is much we still do not know about these very unusual diseases. Who knows what surprises the next 12 months will bring?