Pharmacotherapy for the treatment of tardive dyskinesia in schizophrenia patients.

Tardive dyskinesia (TD) is an iatrogenic movement disorder most commonly observed in patients with psychotic disorders who are treated with dopamine blocking antipsychotic medications. Treatment options are limited, and recommendations for treatment are based on a relative scarcity of evidence. Areas covered: After briefly highlighting current mechanistic theories of TD, this review will discuss the evidence for a number of medications of several different classes that have been studied for the treatment of TD since the 1970s with an emphasis on placebo controlled trials when possible.

A chemical approach for cell-specific targeting of nanomaterials: small-molecule-initiated misfolding of nanoparticle corona proteins.

A major challenge in nanomaterial science is to develop approaches that ensure that when administered in vivo, nanoparticles can be targeted to their requisite site of action. Herein we report the first approach that allows for cell-specific uptake of nanomaterials by a process involving reprogramming of the behavior of the ubiquitous protein corona of nanomaterials. Specifically, judicious surface modification of quantum dots with a small molecule that induces a protein-misfolding event in a component of the nanoparticle-associated protein corona renders the associated nanomaterials susceptible to cell-specific, receptor-mediated endocytosis.

Cholesterol secosterol adduction inhibits the misfolding of a mutant prion protein fragment that induces neurodegeneration.

[Image: see text] Cholesterol sterol aldehydes inhibit the misfolding of a prion protein fragment that induces GSS in mice. Atheronal-B completely inhibits the α to β-form transformation of MoPrP(89-143, P101L) a mechanism that involves adduction to the protein. This result offers a paradigm shift in lipid aldehyde induced protein misfolding and offers a new molecular scaffold on which to develop new potential prion disease therapeutics

The natural products beauveriolide I and III: a new class of beta-amyloid-lowering compounds.

Attacking Alzheimer's by ACAT: The aggregation of beta-amyloid peptides, especially Abeta(42), into senile plaques is a hallmark of Alzheimer's disease (AD). We show that the fungal natural products beauveriolides I and III can potently decrease Abeta secretion from cells expressing human amyloid precursor protein; this offers a potential new scaffold for the development of compounds with proven bioavailability for the treatment of AD.

Proatherogenic effects of the cholesterol ozonolysis products, atheronal-A and atheronal-B.

The proatherogenic properties of the cholesterol 5,6-secosterols (atheronal-A and atheronal-B), recently discovered in atherosclerotic arteries, have been investigated in terms of their effects on monocyte/macrophage function. A fluorescent analogue of atheronal-B (1) (50 microM), when cultured in either aqueous buffer (PBS) or in media containing fetal calf serum (10%), is rapidly taken-up into cultured macrophage (J774.1 or RAW 264.