The demand for biologics such as monoclonal antibodies and vaccines will continue to expand in the US during the next five years, according to predictions in a new industry report. The report, published by the Freedonia Group in Cleveland, Ohio, attributes the predicted annual 6.5 % growth in demand to advances in production technologies and an increasing number of novel disease targets.

“The report analysis is consistent with what we see in market trends, but also in translational research trends,” says Terry Flotte, dean of the University of Massachusetts Medical School and acting head of MassBiologics, a University-associated nonprofit manufacturer of licensed vaccine and biologics.

Biologics are typically engineered biological products such as medicinal proteins. Doctors use them to treat a variety of conditions, such as diabetes, certain cancers and rare genetic diseases like cystic fibrosis.

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Like with any neurodegenerative disorder, treating Alzheimer’s early is key to arresting the disease’s inevitable mental decline. But this is easier said than done. The earliest stages of Alzheimer’s disease — before the symptoms of dementia become apparent — are vague and undefined, and neuroscientists remain divided about how best to characterize the distinct clinical phases of disease progression.

In April, a working group formed by the US National Institute on Aging and the Alzheimer’s Association (NIA-AA) revised the disease’s diagnostic criteria for the first time in 27 years to reflect latest findings about the asymptomatic phases of Alzheimer’s. The group divided cognitively normal people into three stages based on presence of biomarkers in their blood or spinal fluid: a ‘pre-clinical’ phase in which early biomarkers such as beta-amyloid show up but without neurological changes; a second stage showing shrinkage or reduced metabolic activity of neurons and a final stage with gradual cognitive decline, like subtle memory loss.

The diagnostic guidelines were intentionally left vague to allow for updates in the face of emerging data. And less than six months after the criteria came out, a new report has found this trio of stages lacking.

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It’s been a hectic couple of weeks for Judy Mikovits. First, her controversial research on the viral cause of chronic fatigue syndrome was condemned by the journal that published it. Then, her alternative hypothesis — that a new gammaretrovirus closely related to the originally proposed culprit, xenotropic murine leukemia virus-related virus (XMRV), is responsible for chronic fatigue — was received with misgivings by the scientific community at a major international conference. Add to the mix allegations of fabricated results and a blow-out with her boss, and Mikovits ended up being fired from her job at the Whittemore Peterson Institute (WPI) for Neuro-Immune Disease in Reno, Nevada.

The research that spawned the drama was originally published in Science in October 2009, and purported to show a link between the infectious retrovirus XMRV and chronic fatigue syndrome in two-thirds of CFS patients examined. The study, conducted by Mikovits and her collaborators, was the first sign of an infectious cause for the disease. However, follow-up studies since 2009 showed that other labs could not reproduce these results and scientists began to suspect that Mikovits’ original patient samples had been contaminated.

On 22 September, a large study published by Science showed that, of nine national laboratories, none could find XMRV in their patients’ blood — including Mikovits’ own lab. Notably, Science issued a partial retraction of the original 2009 paper on the same day, stating that one of Mikovits’ collaborators had found XMRV contamination in the patient blood samples. The saga was documented in a long feature by Science, ending with Mikovits pledging to continue studying the CFS and its viral links.

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A new mouse model of autism created by scientists at the University of California-Los Angeles promises to mimic the disease more closely than previous animal models, according to a paper out today in the journal Cell. The mice possess the same mutation in the gene contactin associated protein-like 2 (CNTNAP2) seen in a small subset of people with autism. When individuals have two non-functioning versions of the gene, as found in two Amish families, they suffer a suite of symptoms such as epileptic seizures, language regression, hyperactivity and autism. The mice created by the UCLA team exhibit all of these symptoms, including the deficits in vocal communication and repetitive behaviors characteristic of autism linked to CNTNAP2 mutations.

The authors are cautiously optimistic about the new model. “One has to have a caveat that it’s hard to make a direct comparison between human and mouse behavior,” says Daniel Geschwind, the neuropsychiatrist at UCLA who led the investigation.

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