Oyster reef restoration fails to recoup global historic ecosystem losses despite substantial biodiversity gain

This is the final version. Available on open access from the American Association for the Advancement of Science via the DOI in this recordHuman activities have led to degradation of ecosystems globally. The lost ecosystem functions and services accumulate from the time of disturbance to the full recovery of the ecosystem and can be quantified as a "recovery debt," providing a valuable tool to develop better restoration practices that accelerate recovery and limit losses. Here, we quantified the recovery of faunal biodiversity and abundance toward a predisturbed state following structural restoration of oyster habitats globally. We found that while restoration initiates a rapid increase in biodiversity and abundance of reef-associated species within 2 years, recovery rate then decreases substantially, leaving a global shortfall in recovery of 35% below a predisturbed state. While efficient restoration methods boost recovery and minimize recovery shortfalls, the time to full recovery is yet to be quantified. Therefore, potential future coastal development should weigh up not only the instantaneous damage to ecosystem functions but also the potential for generational loss of services.Hong Kong Post-Doctoral FellowshipEnvironment and Conservation Fund Hong KongFaculty of Science (HKU) Rising Star Fun

Gut-brain and brain-gut axis in Parkinson's disease models : Effects of a uridine and fish oil diet

Recent investigations have focused on the potential role of gastrointestinal (GI) abnormalities in the pathogenesis of Parkinson's disease (PD). The 'dual-hit' hypothesis of PD speculates that a putative pathogen enters the brain via two routes: the olfactory system and the GI system. Here, we investigated (1) whether local exposures of the neurotoxin rotenone in the gut or the brain of mice could induce PD-like neurological and GI phenotypes as well as a characteristic neuropathology in accordance with this 'dual-hit hypothesis' and (2) the effects of a diet containing uridine and fish oil providing docosahexaenoic acid (DHA), in both models. Mice were given rotenone either orally or by an injection in the striatum. Dietary interventions were started 1 week before rotenone exposures. We found that (1) both oral and intrastriatal administration of rotenone induced similar PD-like motor deficits, dopaminergic cell loss, delayed intestinal transit, inflammation, and alpha-synuclein accumulation in the colon; (2) the uridine and DHA containing diet prevented rotenone-induced motor and GI dysfunctions in both models. The models suggest possible bidirectional communication between the gut and the brain for the genesis of PD-like phenotype and pathology. The dietary intervention may provide benefits in the prevention of motor and non-motor symptoms in PD