Autonomous Reef Monitoring Structures (ARMS) as a tool to uncover neglected marine biodiversity: two new Solenogastres (Mollusca, Aplacophora) from the Gulf of Mexico.

Solenogastres is a group of mollusks with evolutionary and ecological importance. Nevertheless, their diversity is underestimated and knowledge about the distribution of the approximately 300 formally described species is limited. Factors that contribute to this include their small size and frequent misidentification by non-specialists.

Loss of neprilysin function promotes amyloid plaque formation and causes cerebral amyloid angiopathy.

Cerebral deposition of the amyloid beta protein (Abeta), an invariant feature of Alzheimer's disease, reflects an imbalance between the rates of Abeta production and clearance. The causes of Abeta elevation in the common late-onset form of Alzheimer's disease (LOAD) are largely unknown. There is evidence that the Abeta-degrading protease neprilysin (NEP) is down-regulated in normal aging and LOAD.

Effects of prolonged angiotensin-converting enzyme inhibitor treatment on amyloid beta-protein metabolism in mouse models of Alzheimer disease.

Genetic and pathologic studies have associated angiotensin-converting enzyme (ACE) with Alzheimer disease. Previously, we and others have reported that ACE degrades in vitro the amyloid beta-protein (Abeta), a putative upstream initiator of Alzheimer disease. These studies support the hypothesis that deficiency in ACE-mediated Abeta proteolysis could increase Alzheimer disease risk and raise the question of whether ACE inhibitors, a commonly prescribed class of anti-hypertensive medications, can elevate Abeta levels in vivo.

Decreased catalytic activity of the insulin-degrading enzyme in chromosome 10-linked Alzheimer disease families.

Insulin-degrading enzyme (IDE) is a zinc metalloprotease that degrades the amyloid beta-peptide, the key component of Alzheimer disease (AD)-associated senile plaques. We have previously reported evidence for genetic linkage and association of AD on chromosome 10q23-24 in the region harboring the IDE gene. Here we have presented the first functional assessment of IDE in AD families showing the strongest evidence of the genetic linkage.

Alternative splicing of human insulin-degrading enzyme yields a novel isoform with a decreased ability to degrade insulin and amyloid beta-protein.

Deletion of insulin-degrading enzyme (IDE) in mice causes accumulation of cerebral amyloid beta-protein (Abeta), hyperinsulinemia, and glucose intolerance. Together with genetic linkage and allelic association of IDE to Alzheimer's disease (AD) and type 2 diabetes mellitus (DM2), these findings suggest that IDE hypofunction could mediate human disease. To date, no coding mutations have been found in the canonical isoform of IDE, suggesting that pathological mutations could exist in undiscovered exons or regulatory regions, including untranslated regions (UTRs).