Centrally Delivered BACE1 Inhibitor Activates Microglia, and Reverses Amyloid Pathology and Cognitive Deficit in Aged Tg2576 Mice.

Multiple small-molecule inhibitors of the β-secretase enzyme (BACE1) are under preclinical or clinical investigation for Alzheimer's disease (AD). Prior work has illustrated robust lowering of central amyloid β (Aβ) after acute administration of BACE1 inhibitors. However, very few studies have assessed the overall impact of chronically administered BACE1 inhibitors on brain amyloid burden, neuropathology, and behavioral function in aged preclinical models.

[Conservative treatment strategies for gonarthritis. New trends and established therapy concepts].

This article gives a current overview of non-operative procedures in cases of osteoarthritis of the knee, e.g. with special medications, local physiotherapy and gymnastic therapy including ergotherapy and aids for activities of daily living (ADL).

Safety and efficacy findings from a non-interventional study of a new hyaluronic acid/sorbitol formulation (GO-ON® matrix) for intra-articular injection to relieve pain and disability in osteoarthritis patients.

This non-interventional study was intended to examine the efficacy and tolerability of intra-articular injections with the GO-ON® matrix, a new viscosupplement product made of non-animal sodium hyaluronate combined with the oxygen free radical scavenger sorbitol, when used in routine clinical practice. A total of 1 147 patients (43.5% male, 53,5% female, 3% missing) aged on average 63.

[Postoperative rehabilitation after minimally invasive total hip arthroplasty].

Currently more than 150,000 total hip arthroplasties (THA) are performed in Germany each year. Despite limited financial resources approximately 50% of these patients participate in a standardized inpatient rehabilitation program. This report reflects own experiences with patients after a minimally invasive approach for THA compared to others with conventional procedures, in context with findings from the literature.

Six-month partial suppression of Huntingtin is well tolerated in the adult rhesus striatum.

Huntington's disease is caused by expression of a mutant form of Huntingtin protein containing an expanded polyglutamine repeat. One possible treatment for Huntington's disease may be to reduce expression of mutant Huntingtin in the brain via RNA interference. Unless the therapeutic molecule is designed to be allele-specific, both wild-type and mutant protein will be suppressed by an RNA interference treatment.