Differential responses of zooplankton assemblages to environmental variation in temporary and permanent ponds

Permanent and temporary wetlands in Mediterranean shrublands represent unique repositories of biodiversity, which are increasingly threatened by human-induced habitat loss. The zooplankton of a permanent (P1) and a temporary pond (T35) in the Natural Reserve of Castelporziano, a rare residual stretch of such a shrubland in Central Italy (Latium), was investigated to: (1) expand and deepen knowledge of these endangered freshwater habitats, which represent a crucial component of Mediterranean biodiversity; (2) identify environmental controls regulating the development of zooplankton communities of each environment; and (3) highlight differences in the adaptive responses of the zooplankton community in relation to the different ecological conditions experienced by permanent and temporary habitats. Despite summer desiccation in T35, the two ponds exhibited a relative homogeneity in hydrological and physico-chemical dynamics. Zooplankton assemblages contained 41 total taxa, of which 32 were found in P1 and 28 in T35. Out of the 41 taxa identified, 22 (> 50%) were exclusively present in one of the two ponds. On a yearly basis, the community dynamics of P1 seemed to be conditioned by physical and chemical factors and by hydrological cycle characteristics, while the community of T35 responded to algal blooms, food competition and predator/prey equilibria rather than correlating to abiotic factors. The main differences amongst zooplankton assemblages were observed over short time scales and occurred both within and between seasons, highlighting the role of some structural taxa that dominated the average composition of the community throughout the year, and the importance of "quick-response" taxa in determining the short-term composition and structure variation of pond zooplankton. A year-round cyclic community succession peculiar to each pond is described

Hippocampal pyramidal cells: the reemergence of cortical lamination

The increasing resolution of tract-tracing studies has led to the definition of segments along the transverse axis of the hippocampal pyramidal cell layer, which may represent functionally defined elements. This review will summarize evidence for a morphological and functional differentiation of pyramidal cells along the radial (deep to superficial) axis of the cell layer. In many species, deep and superficial sublayers can be identified histologically throughout large parts of the septotemporal extent of the hippocampus. Neurons in these sublayers are generated during different periods of development. During development, deep and superficial cells express genes (Sox5, SatB2) that also specify the phenotypes of superficial and deep cells in the neocortex. Deep and superficial cells differ neurochemically (e.g. calbindin and zinc) and in their adult gene expression patterns. These markers also distinguish sublayers in the septal hippocampus, where they are not readily apparent histologically in rat or mouse. Deep and superficial pyramidal cells differ in septal, striatal, and neocortical efferent connections. Distributions of deep and superficial pyramidal cell dendrites and studies in reeler or sparsely GFP-expressing mice indicate that this also applies to afferent pathways. Histological, neurochemical, and connective differences between deep and superficial neurons may correlate with (patho-) physiological phenomena specific to pyramidal cells at different radial locations. We feel that an appreciation of radial subdivisions in the pyramidal cell layer reminiscent of lamination in other cortical areas may be critical in the interpretation of studies of hippocampal anatomy and function

Identification and Validation of Novel Cerebrospinal Fluid Biomarkers for Staging Early Alzheimer's Disease

Ideally, disease modifying therapies for Alzheimer disease (AD) will be applied during the 'preclinical' stage (pathology present with cognition intact) before severe neuronal damage occurs, or upon recognizing very mild cognitive impairment. Developing and judiciously administering such therapies will require biomarker panels to identify early AD pathology, classify disease stage, monitor pathological progression, and predict cognitive decline. To discover such biomarkers, we measured AD-associated changes in the cerebrospinal fluid (CSF) proteome.CSF samples from individuals with mild AD (Clinical Dementia Rating [CDR] 1) (n = 24) and cognitively normal controls (CDR 0) (n = 24) were subjected to two-dimensional difference-in-gel electrophoresis. Within 119 differentially-abundant gel features, mass spectrometry (LC-MS/MS) identified 47 proteins. For validation, eleven proteins were re-evaluated by enzyme-linked immunosorbent assays (ELISA). Six of these assays (NrCAM, YKL-40, chromogranin A, carnosinase I, transthyretin, cystatin C) distinguished CDR 1 and CDR 0 groups and were subsequently applied (with tau, p-tau181 and Aβ42 ELISAs) to a larger independent cohort (n = 292) that included individuals with very mild dementia (CDR 0.5). Receiver-operating characteristic curve analyses using stepwise logistic regression yielded optimal biomarker combinations to distinguish CDR 0 from CDR>0 (tau, YKL-40, NrCAM) and CDR 1 from CDR<1 (tau, chromogranin A, carnosinase I) with areas under the curve of 0.90 (0.85-0.94 95% confidence interval [CI]) and 0.88 (0.81-0.94 CI), respectively.Four novel CSF biomarkers for AD (NrCAM, YKL-40, chromogranin A, carnosinase I) can improve the diagnostic accuracy of Aβ42 and tau. Together, these six markers describe six clinicopathological stages from cognitive normalcy to mild dementia, including stages defined by increased risk of cognitive decline. Such a panel might improve clinical trial efficiency by guiding subject enrollment and monitoring disease progression. Further studies will be required to validate this panel and evaluate its potential for distinguishing AD from other dementing conditions

The temporal dynamics of temporary pond macroinvertebrate communities over a 10-year period

Ponds support a rich biodiversity. This arises in part because of the number and heterogeneity of ponds spatially throughout the landscape. Studies of ponds suggest that distinct communities develop within individual ponds but most examples are based on shortterm 1- or 2-year surveys which cannot identify the effects of historic events upon contemporary communities. This study reports the development and turnover of the early summer macroinvertebrate communities in thirty small temporary ponds fromtheir creation in 1994 over 10 years to 2004. Distinct pioneer communities established in the first year of the ponds’ creation, the first 3 years dominated by a fauna associated with long summer dry phases. Then a sustained period of inundation lasting 27 months from summer 1997–1999 resulted in establishment of many taxa associated with permanent ponds and loss of some temporary pond species. The re-establishment of summer dry phases in 1999 was associated with the loss of some but not all of the permanent water taxa and re-colonisation by some temporary water species creating new communities combining these different elements. The communities were not a linear successional sequence; the communities that re-assembled following resumption of dry phases reflected the contingent history of each pond and the effects of historic events. The longer term nature of the study showed that the characteristic heterogeneity of pond invertebrate communities occurs through time as well as spatially and that the richness and variety of contemporary communities, which is often hard to explain fromsnap-shot studies, is partly the result of historic events

Demyelination in mild cognitive impairment suggests progression path to Alzheimer's disease.

The preclinical Alzheimer's disease (AD) - amnestic mild cognitive impairment (MCI) - is manifested by phenotypes classified into exclusively memory (single-domain) MCI (sMCI) and multiple-domain MCI (mMCI). We suggest that typical MCI-to-AD progression occurs through the sMCI-to-mMCI sequence as a result of the extension of initial pathological processes. To support this hypothesis, we assess myelin content with a Magnetization Transfer Ratio (MTR) in 21 sMCI and 21 mMCI patients and in 42 age-, sex-, and education-matched controls. A conjunction analysis revealed MTR reduction shared by sMCI and mMCI groups in the medial temporal lobe and posterior structures including white matter (WM: splenium, posterior corona radiata) and gray matter (GM: hippocampus; parahippocampal and lingual gyri). A disjunction analysis showed the spread of demyelination to prefrontal WM and insula GM in executive mMCI. Our findings suggest that demyelination starts in the structures affected by neurofibrillary pathology; its presence correlates with the clinical picture and indicates the method of MCI-to-AD progression. In vivo staging of preclinical AD can be developed in terms of WM/GM demyelination