Friday, March 16, 2012

Upcoming Event: "Does the Brainʼs Wiring Make Us Who We Are?" (02 April 2012, NYC)

Does the brainʼs wiring make us who we are?
Event homepage

And, as discussed by Carl Zimmer:
The Loom

Neuroscience in Seattle

The Greater Seattle Brain Science Cluster
xconomy.com
Luke Timmerman
16 March 2012

Read article

Wednesday, March 14, 2012

FDA: Generic Lexapro

A press release from the FDA:

FDA approves first generic Lexapro to treat depression and anxiety disorder
14 March 2012

Read the full press release

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Monday, March 12, 2012

Memory: BDNF and microRNAs

Making memories: How one protein does it
The JHU Gazette
12 March 2012

[snip]

"Studying tiny bits of genetic material that control protein formation in the brain, Johns Hopkins scientists say that they have new clues to how memories are made and how drugs might someday be used to stop disruptions in the process that lead to mental illness and brain-wasting diseases.

"In a report published in the March 2 issue of Cell, the researchers say that certain microRNAs—genetic elements that control which proteins get made in cells—are the key to controlling the actions of so-called brain-derived neurotrophic factor, or BDNF, long linked to brain cell survival, normal learning and memory boosting."
[snip]

Read the full article

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Sunday, March 11, 2012

Brain Awareness Week is Here!




Visit the Brain Awareness Week homepage at the Dana Foundation!

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Saturday, March 03, 2012

Computerized Cognitive Testing

I noticed the abstract for this new paper earlier in the day. It should be a good read.

Bauer RM, Iverson GL, Cernich AN, Binder LM, Ruff RM, Naugle RI (2012). Computerized neuropsychological assessment devices: Joint position paper of the American Academy of Clinical Neuropsychology and the National Academy of Neuropsychology.
Archives of Clinical Neuropsychology (2012 Mar 1).

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Neuropsychological Abstract of the Day: Alzheimer Clinical Trial

Multicenter, Randomized, Double-Blind, Placebo-Controlled, Single-Ascending Dose Study of the Oral γ-Secretase Inhibitor BMS-708163 (Avagacestat): Tolerability Profile, Pharmacokinetic Parameters, and Pharmacodynamic Markers
Clin Ther. 2012 Feb 28;
Tong G, Wang JS, Sverdlov O, Huang SP, Slemmon R, Croop R, Castaneda L, Gu H, Wong O, Li H, Berman RM, Smith C, Albright CF, Dockens RC

Abstract

BACKGROUND: γ-Secretase inhibitors (GSIs) are being investigated for their potential to modify the progression of Alzheimer disease based on their ability to regulate amyloid-β (Aβ) accumulation. BMS-708163 (avagacestat) is an oral GSI designed for selective inhibition of Aβ synthesis currently in development for the treatment of mild to moderate and predementia AD. In addition to the desired effect on Aβ synthesis, GSIs affect Notch processing, which is thought to mediate some toxic adverse effects reported with this drug class. Avagacestat produced up to 190-fold greater selectivity for Aβ synthesis than Notch processing in preclinical studies and may therefore produce less toxic adverse events than other less selective compounds. Presented here are the results of the first in-human study for this new GSI compound. OBJECTIVE: The goal of this study was to assess the tolerability profile, pharmacokinetic properties, and effects on pharmacodynamic markers (Aβ, trefoil factor family 3 protein, dual specificity phosphatase 6, and hairy and enhancer of split-1) of single, oral doses of avagacestat in healthy, young, male volunteers. METHODS: This was a multicenter, randomized, double-blind, placebo-controlled, single-ascending dose study in 8 healthy young men (age, 18-45 years) per dosing panel. Each study participant was randomized to receive a single dose of placebo (n = 2) or avagacestat (n = 6 for each dose) as an oral solution in 1 of 9 sequential dose panels (0.3, 1.5, 5, 15, 50, 100, 200, 400, and 800 mg). For determination of avagacestat, blood samples were obtained before dosing and for up to 144 hours after dosing. For participants in the 800-mg avagacestat dose panel, additional samples were obtained at 216, 312, and 648 hours. For 40-amino acid isoform of Aβ (Aβ(1-40)) assessment, plasma samples were collected before avagacestat administration and up to 72 hours after dosing. RESULTS: Avagacestat concentrations peaked quickly after oral administration and then had a biphasic decrease in concentrations with a prolonged terminal phase. Exposures were proportional with doses up to 200 mg. Avagacestat was well tolerated at single oral doses up to 800 mg, with a biphasic effect on plasma Aβ(1-40). Adverse events were predominately mild to moderate in severity with no evidence of dose dependence up to 200 mg. CONCLUSIONS: Results from this single-ascending dose study suggest that avagacestat was tolerated at a single-dose range of 0.3 to 800 mg and suitable for further clinical development.

ClinicalTrials.gov identifier: NCT01454115.

PMID: 22381714 [PubMed - as supplied by publisher]

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