Impacts of urbanisation on the native avifauna of Perth, Western Australia

Urban development either eliminates, or severely fragments, native vegetation, and therefore alters the distribution and abundance of species that depend on it for habitat. We assessed the impact of urban development on bird communities at 121 sites in and around Perth, Western Australia. Based on data from community surveys, at least 83 % of 65 landbirds were found to be dependent, in some way, on the presence of native vegetation. For three groups of species defined by specific patterns of habitat use (bushland birds), there were sufficient data to show that species occurrences declined as the landscape changed from variegated to fragmented to relictual, according to the percentage of vegetation cover remaining. For three other groups (urban birds) species occurrences were either unrelated to the amount of vegetation cover, or increased as vegetation cover declined. In order to maximise the chances of retaining avian diversity when planning for broad-scale changes in land-use (i.e. clearing native vegetation for housing or industrial development), land planners should aim for a mosaic of variegated urban landscapes (\u3e60 % vegetation retention) set amongst the fragmented and relictual urban landscapes (% vegetation retention) that are characteristic of most cities and their suburbs. Management actions for conserving remnant biota within fragmented urban landscapes should concentrate on maintaining the integrity and quality of remnant native vegetation, and aim at building awareness among the general public of the conservation value of remnant native vegetation

Genetically-controlled Vesicle-Associated Membrane Protein 1 expression may contribute to Alzheimer’s pathophysiology and susceptibility

Background Alzheimer’s disease is a neurodegenerative disorder in which extracellular deposition of β-amyloid (Aβ) oligomers causes synaptic injury resulting in early memory loss, altered homeostasis, accumulation of hyperphosphorylated tau and cell death. Since proteins in the SNAP (Soluble N-ethylmaleimide-sensitive factor Attachment Protein) REceptors (SNARE) complex are essential for neuronal Aβ release at pre-synaptic terminals, we hypothesized that genetically controlled SNARE expression could alter neuronal Aß release at the synapse and hence play an early role in Alzheimer’s pathophysiology. Results Here we report 5 polymorphisms in Vesicle-Associated Membrane Protein 1 (VAMP1), a gene encoding a member of the SNARE complex, associated with bidirectionally altered cerebellar VAMP1 transcript levels (all p < 0.05). At the functional level, we demonstrated that control of VAMP1 expression by heterogeneous knockdown in mice resulted in up to 74% reduction in neuronal Aβ exocytosis (p < 0.001). We performed a case-control association study of the 5 VAMP1 expression regulating polymorphisms in 4,667 Alzheimer’s disease patients and 6,175 controls to determine their contribution to Alzheimer’s disease risk. We found that polymorphisms associated with increased brain VAMP1 transcript levels conferred higher risk for Alzheimer’s disease than those associated with lower VAMP1 transcript levels (p = 0.03). Moreover, we also report a modest protective association for a common VAMP1 polymorphism with Alzheimer’s disease risk (OR = 0.88, p = 0.03). This polymorphism was associated with decreased VAMP1 transcript levels (p = 0.02) and was functionally active in a dual luciferase reporter gene assay (p < 0.01). Conclusions Genetically regulated VAMP1 expression in the brain may modify both Alzheimer’s disease risk and may contribute to Alzheimer’s pathophysiology

Genome-wide association study of primary open-angle glaucoma in continental and admixed African populations

Contains fulltext : 200131.pdf (publisher's version ) (Open Access)Primary open angle glaucoma (POAG) is a complex disease with a major genetic contribution. Its prevalence varies greatly among ethnic groups, and is up to five times more frequent in black African populations compared to Europeans. So far, worldwide efforts to elucidate the genetic complexity of POAG in African populations has been limited. We conducted a genome-wide association study in 1113 POAG cases and 1826 controls from Tanzanian, South African and African American study samples. Apart from confirming evidence of association at TXNRD2 (rs16984299; OR[T] 1.20; P = 0.003), we found that a genetic risk score combining the effects of the 15 previously reported POAG loci was significantly associated with POAG in our samples (OR 1.56; 95% CI 1.26-1.93; P = 4.79 x 10(-5)). By genome-wide association testing we identified a novel candidate locus, rs141186647, harboring EXOC4 (OR[A] 0.48; P = 3.75 x 10(-8)), a gene transcribing a component of the exocyst complex involved in vesicle transport. The low frequency and high degree of genetic heterogeneity at this region hampered validation of this finding in predominantly West-African replication sets. Our results suggest that established genetic risk factors play a role in African POAG, however, they do not explain the higher disease load. The high heterogeneity within Africans remains a challenge to identify the genetic commonalities for POAG in this ethnicity, and demands studies of extremely large size