Public Release: 

The Lancet Neurology November press release

No sex please, we're British (neurologists)

Lancet

It is well known in media circles that including the word "sex" in a headline is a sure-fire way of attracting the attention of potential readers. It is understandable, therefore, why a paper published in the Journal of Neurology, Neurosurgery, and Psychiatry (JNNP) entitled "Is multiple sclerosis a sexually transmitted infection?" was well covered by the UK media on Sept 19. Unfortunately, however, the news stories understandably upset many patients with multiple sclerosis. This month's Leading edge (http://neurology.thelancet.com/journal/vol1/iss7/full/lneu.1.7.the_leading_edge.22731.1) discusses who, if anyone, was to blame for this and asks what the lay media, academic journals, scientists, and the general public should expect from each other.

Cyclo-oxygenase inhibitors and Alzheimer's: are we well adapted?

On Sept 4, 2002, the Public Citizen Health Research Group (PCHRG; Washington, DC, USA) sent a letter to US Secretary of Health and Human Services, Tommy Thompson, regarding the Alzheimer's Disease Anti-Inflammatory Prevention Trial (ADAPT), which is sponsored by the National Institute on Aging. In the letter, PCHRG called ADAPT "misleading and incomplete..." and said that there are "major problems...with the scientific premise upon which the study is based". In a Reflection and Reaction article (http://neurology.thelancet.com/journal/vol1/iss7/full/lneu.1.7.reflection_and_reaction.22777.1) Giulio Maria Pasinetti and colleagues (Neuroinflammation Research Laboratories, Mount Sinai School of Medicine, New York, USA) summarise the recent evidence supporting preventative anti-inflammatory clinical trials in Alzheimer's disease,and objectively revisit the key studies cited by PCHRG. The authors commentary reinforces the scientific premise of the ADAPT, and disputes the concerns raised by the PCHAG letter.

Secretases as targets for the treatment of Alzheimer's disease: the prospects

Abnormal accumulation of amyloid-beta peptide into extracellular plaques is thought to be responsible for the neurodegeneration and dementia seen in Alzheimer's disease. Amyloid-beta peptide is produced from the much larger amyloid precursor protein (APP) by the action of enzymes called "secretases". These enzymes are possible therapeutic targets to prevent or slow the onset of Alzheimer's disease. A review (http://neurology.thelancet.com/journal/vol1/iss7/abs/lneu.1.7.review_and_opinion.22749.1) by Ilse Dewachter and Fred Van Leuven (KU Leuven, Leuven, Belgium) discusses the rationale behind this approach.

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Other reviews:

  • Neuroimaging, the ischaemic penumbra, and selection of patients for acute stroke therapy
  • Subcortical ischaemic vascular dementia
  • Santiago Ramón y Cajal and the Spanish school of neurology
  • The hypothalamus in episodic brain disorders
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