1,721,034 research outputs found
Young Blood Plasma Administration to Fight Alzheimer's Disease?
No full textDespite decades of intensive research, no drugs can cure or even stabilize Alzheimer's disease (AD). Current pharmacological treatments only partially mask the symptoms while the disease progresses within the brain. Finding a preventive measure or a cure for people with AD is indeed a worldwide urgent priority. A recent interesting study by T. Wyss-Coray's research group provides the first evidence that exposure to young blood or plasma can reverse some AD-related molecular and behavioral alterations. Heterochronic parabiosis (shared blood circulation) of AD transgenic mice with young healthy mice did not reduce amyloidosis and microglial activation in AD mice, but reversed the loss of synaptophysin and calbindin (critical synaptic proteins, indicators of cognitive decline in AD) in the dentate gyrus, and the abnormal expression, in the hippocampus, of many genes involved in key neuronal signaling pathways. Moreover, repeated intravenous administration of plasma from young healthy mice to AD mice reversed the excessive phosphorylation of hippocampal extracellular signal-regulated kinase (ERK), and improved spatial working memory and associative memory. Although observations in mouse models of AD might not necessarily extrapolate to humans, this preclinical study provides the first demonstration that young plasma has potential therapeutic properties, by ameliorating aspects of the disease that are present in AD patients. Clinical trials are already under way. If young plasma transfusion will be effective in AD patients, it will be important to identify the key factors responsible for the positive effects, as they might lead to the development of molecule interventions with a better efficacy/risk profile
Hypoxia Depresses Synaptic Transmission in the Primary Motor Cortex of the Infant Rat—Role of Adenosine A1 Receptors and Nitric Oxide
Full text linkThe acute and long-term consequences of perinatal asphyxia have been extensively investigated, but only a few studies have focused on postnatal asphyxia. In particular, electrophysiological changes induced in the motor cortex by postnatal asphyxia have not been examined so far, despite the critical involvement of this cortical area in epilepsy. In this study, we exposed primary motor cortex slices obtained from infant rats in an age window (16–18 day-old) characterized by high incidence of hypoxia-induced seizures associated with epileptiform motor behavior to 10 min of hypoxia. Extracellular field potentials evoked by horizontal pathway stimulation were recorded in layers II/III of the primary motor cortex before, during, and after the hypoxic event. The results show that hypoxia reversibly depressed glutamatergic synaptic transmission and neuronal excitability. Data obtained in the presence of specific blockers suggest that synaptic depression was mediated by adenosine acting on pre-synaptic A1 receptors to decrease glutamate release, and by a nitric oxide (NO)/cGMP postsynaptic pathway. These effects are neuroprotective because they limit energy failure. The present findings may be helpful in the preclinical search for therapeutic strategies aimed at preventing acute and long-term neurological consequences of postnatal asphyxia
Role of nitric oxide and endocannabinoids in synaptic plasticity in the perirhinal cortex
No full textNitric oxide (NO) and endocannabinoids (eCBs) are major retrograde messengers that are involved in synaptic plasticity as well as in learning and memory. NO mainly exerts its functions through soluble guanylate cyclase (sGC) activation. Activity-dependent release of eCBs in the central nervous system leads to the activation of the Gi/o-coupled cannabinoid receptor 1 (CB1) at both excitatory and inhibitory synapses.
The perirhinal cortex (Prh) is a multimodal associative cortex of the temporal lobe, critically involved in recognition memory. Long-term depression (LTD) is proposed to be the cellular correlate underlying this form of memory. Cholinergic neurotransmission plays a critical role in both visual recognition memory and LTD in Prh. The aim of the present research was to investigate the role of NO and ECBs in synaptic plasticity in rat Prh.
Extracellular field potential recordings were carried out in horizontal Prh slices from Sprague-Dawley or Dark Agouti (p21-35) rats. LTD was induced with a single train of 3000 pulses at 5 Hz, or via bath application of carbachol (Cch; 50 μM) for 10 min. Long-term potentiation (LTP) was induced by theta-burst stimulation (TBS).
We found that 5Hz-LTD and Cch-LTD induction rely on the activation of the NOS/sGC pathway but not on CB1. By contrast, TBS-LTP was shown to require CB1 but not NOS activation. These results demonstrate that distinct retrograde signalling underlies different forms of synaptic plasticity in the perirhinal cortex
FELS, Greulich-Pyle, and Tanner-Whitehouse bone age assessments in a group of Italian children and adolescents
No full text
Use of the new US90 standards for TW-RUS skeletal maturity scores in youths from the Italian population
No full textEarly impairment of long-term depression in the perirhinal cortex of Tg2576 mice
No full textThe Tg2576 Alzheimer’s disease (AD) mouse line shows a marked increase in amyloid-β (Aβ) 1–40 and Aβ1–42 in the plasma and brain by 3–5 months of age, decrease in spine density in the dentate gyrus at 4 months, decline in long-term potentiation of synaptic transmission in the dentate gyrus associated with impairment in contextual fear conditioning by 5 months, and plaque deposition in brain starting at 8 months. Visual recognition memory is seriously impaired in patients in the early stages of AD. The perirhinal cortex (Prh), a multimodal associative cortex of the temporal lobe, is critically involved in this form of memory; long-term depression of synaptic transmission (LTD) in this cortical region is regarded as its cellular correlate. The present work was aimed at evaluating if LTD in Prh of Tg2576 mice is already compromised at 3 months of age. Field excitatory post-synaptic potentials evoked by afferent pathways stimulation were recorded in layer II/III of Prh in horizontal brain slices obtained from 3 month old Tg2576 mice and littermate controls. We found that a single train of 3000 pulses delivered at 5 Hz induced LTD in slices from control mice, but not in those from Tg2576 mice. This result is consistent with the early visual recognition impairment observed in AD patients, and is particularly interesting because no changes in synaptic plasticity have previously been found so early in this transgenic line
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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