Kiwi boffins prove that booze makes you clever

Two or three a day for a healthy brain, like it or not!

At last, scientists have delivered conclusive proof of what many people instinctively knew - booze makes you clever.

Top boffins at the University of Auckland, New Zealand, by studying the mental performance of specially-created transgenic rats well supplied with drink, have found that moderate daily alcohol intake conferred "heightened cognition".

Kiwi brainbox Maggie Kalev said she "thought it was worth pursuing, since ethanol drinking is such a common pattern of human behaviour... This is similar to a glass of wine protecting against heart disease, however the mechanism is different".

Scientific American covered the pleasing biological breakthrough last week, under the headline "Don't forget: Drink a Beer - or Two - Daily!"

That, of course, is excellent health advice; now backed up by cutting edge Kiwi genetically modified alco-rat research. But in fact it doesn't have to be beer, and Kalev says the brain-enhancement effects kick in at "approximately one to two drinks per day for some people or two to three for others, depending upon their size, metabolism, or genetic background" - based on the equivalent blood alcohol levels to those found in her thirsty mutant rats, anyway.

It seems the rats were separated into three groups. One was put on a fairly hefty booze intake equivalent to five or six beers a day; another lot got a ration "equivalent to a level of consumption that does not exceed [the] legal driving limit" - though disappointingly they still were not allowed to drive cars. The third, luckless group of rodents were put on a temperance regime.

After four weeks of heavy, moderate, or no drinking, the rats were tested to see how their brains had been affected. Unsurprisingly, the most alcoholic rats showed signs of impairment, seeming unable to recognise familiar ratty toys. According to SciAm, the booziest murines also exhibited the symptoms of the lachrymose drunk. They "performed better than their normal brethren on the emotional memory task", suggesting that they had started to ramble on tiresomely to the other rats about their ex-wives or similar.

"People often drink to 'drown sorrows'," according to Kalev. "Our results suggest that this could actually paradoxically promote traumatic memories and lead to further drinking, contributing to the development of alcoholism."

So remember - drinking is for happy occasions, not sad ones.

The greatest revelations, however, came with the moderately-thirsty group who had the equivalent of two of three cheery ales a day. These upstanding correctly-lifestyled rats trounced the teetotallers in every area.

One test in particular involved the small furry Kiwis being given an electric shock whenever they walked on a black-coloured area inside a cage. Faculties unhinged by a steady regimen of tea and fruit juice, the third group were unable to remember that the black area was painful, paying a grisly electric price for their abstinence.

Regrettably, however, it appeared that in the case of alcohol brain therapy more is not better. Boffins were agreed that drinking a lot is - couterintuitively, perhaps - actually worse for you than having no booze at all. But having no booze is bad too; which means that po-faced killjoys who want to put up the already outrageous grog taxes are effectively saying that only the rich can be clever.

So the best thing is to have a couple of beers each and every day without fail, even if you don't want them. Or you could have wine instead, and so benefit your heart as well as your brain. Skipping days is bad for you; especially if you then try to catch up later and drink several days' dose of brain-booster in a oner.

http://www.theregister.co.uk/2007/10/03/kiwi_boffins_prove_booze_makes_you_clever/

All I can do is L O L

Discovery supports theory of Alzheimer's disease as form of diabetes

Insulin, it turns out, may be as important for the mind as it is for the body. Research in the last few years has raised the possibility that Alzheimer’s memory loss could be due to a novel third form of diabetes.
Now scientists at Northwestern University have discovered why brain insulin signaling -- crucial for memory formation -- would stop working in Alzheimer’s disease. They have shown that a toxic protein found in the brains of individuals with Alzheimer’s removes insulin receptors from nerve cells, rendering those neurons insulin resistant. (The protein, known to attack memory-forming synapses, is called an ADDL for “amyloid ß-derived diffusible ligand.”)

With other research showing that levels of brain insulin and its related receptors are lower in individuals with Alzheimer’s disease, the Northwestern study sheds light on the emerging idea of Alzheimer’s being a “type 3” diabetes.

The new findings, published online by the FASEB Journal, could help researchers determine which aspects of existing drugs now used to treat diabetic patients may protect neurons from ADDLs and improve insulin signaling in individuals with Alzheimer’s. (The FASEB Journal is a publication of the Federation of American Societies for Experimental Biology.)

In the brain, insulin and insulin receptors are vital to learning and memory. When insulin binds to a receptor at a synapse, it turns on a mechanism necessary for nerve cells to survive and memories to form. That Alzheimer’s disease may in part be caused by insulin resistance in the brain has scientists asking how that process gets initiated.

“We found the binding of ADDLs to synapses somehow prevents insulin receptors from accumulating at the synapses where they are needed,” said William L. Klein, professor of neurobiology and physiology in the Weinberg College of Arts and Sciences, who led the research team. “Instead, they are piling up where they are made, in the cell body, near the nucleus. Insulin cannot reach receptors there. This finding is the first molecular evidence as to why nerve cells should become insulin resistant in Alzheimer’s disease.”

ADDLS are small, soluble aggregated proteins. The clinical data strongly support a theory in which ADDLs accumulate at the beginning of Alzheimer’s disease and block memory function by a process predicted to be reversible.

In earlier research, Klein and colleagues found that ADDLs bind very specifically at synapses, initiating deterioration of synapse function and causing changes in synapse composition and shape. Now Klein and his team have shown that the molecules that make memories at synapses -- insulin receptors -- are being removed by ADDLs from the surface membrane of nerve cells.

“We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer’s brains,” said Klein, a member of Northwestern’s Cognitive Neurology and Alzheimer's Disease Center. “We’re dealing with a fundamental new connection between two fields, diabetes and Alzheimer’s disease, and the implication is for therapeutics. We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult.”

Using mature cultures of hippocampal neurons, Klein and his team studied synapses that have been implicated in learning and memory mechanisms. The extremely differentiated neurons can be investigated at the molecular level. The researchers studied the synapses and their insulin receptors before and after ADDLs were introduced.

They discovered the toxic protein causes a rapid and significant loss of insulin receptors from the surface of neurons specifically on dendrites to which ADDLs are bound. ADDL binding clearly damages the trafficking of the insulin receptors, preventing them from getting to the synapses. The researchers measured the neuronal response to insulin and found that it was greatly inhibited by ADDLs.

“In addition to finding that neurons with ADDL binding showed a virtual absence of insulin receptors on their dendrites, we also found that dendrites with an abundance of insulin receptors showed no ADDL binding,” said co-author Fernanda G. De Felice, a visiting scientist from Federal University of Rio de Janeiro who is working in Klein’s lab. “These factors suggest that insulin resistance in the brains of those with Alzheimer’s is a response to ADDLs.”

“With proper research and development the drug arsenal for type 2 diabetes, in which individuals become insulin resistant, may be translated to Alzheimer’s treatment,” said Klein. “I think such drugs could supercede currently available Alzheimer’s drugs.”

Source: Northwestern University

http://www.physorg.com/news110029762.html