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The conclusion is that the high-fat diet triggered chronic inflammation, which in turn triggered an autoimmune response in the mice's central nervous systems. Normally this response protects the brain from invaders like bacteria, but a high-saturated fat diet knocks the process off track, resulting in damage to synapses in the brain - specifically in the hippocampus. Since the hippocampus is a brain area central to memory and learning, the eventual outcome is impaired brain function. In short, the high-fat diet caused brain damage.

Scientists and clinicians have demonstrated that a neuroprotectant drug protects the human brain against the damaging effects of stroke. In patients who had ruptured brain aneurysm, which comprise a population of patients at very high risk of neurological damage, those treated with Tat-NR2B9c all had good neurological outcomes, whereas only 68% of those treated with placebo had good outcomes.

The study is the first to examine all of the gene networks affected by fructose that result in changes to brain function and metabolism-more than 20,000 genes in total. Although the study was conducted using rats, the researchers report that the majority of the sequenced genes are comparable to those in humans, including more than 200 genes in the hippocampus, a brain area crucial to memory, and 700 in the hypothalamus, the seat of the brain's metabolic control center.

Multiple sclerosis is an autoimmune condition in which components of the immune system mistakenly attack the fatty lining around nerves in the brain and spinal cord. The majority of drugs currently used to tackle the symptoms of MS, therefore, focus on preventing this destruction by targeting the immune system. But a team of scientists think they may have found a different approach to treatment: targeting stem cells already present in the patient's nervous system.

For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone-the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures.