Sleep directly following learning benefits consolidation of spatial associative memory

Contains fulltext : 128176.pdf (publisher's version ) (Open Access)The last decade has brought forth convincing evidence for a role of sleep in non-declarative memory. A similar function of sleep in episodic memory is supported by various correlational studies, but direct evidence is limited. Here we show that cued recall of face–location associations is significantly higher following a 12-h retention interval containing sleep than following an equally long period of waking. Furthermore, retention is significantly higher over a 24-h sleep–wake interval than over an equally long wake–sleep interval. This difference occurs because retention during sleep was significantly better when sleep followed learning directly, rather than after a day of waking. These data demonstrate a beneficial effect of sleep on memory that cannot be explained solely as a consequence of reduced interference. Rather, our findings suggest a competitive consolidation process, in which the fate of a memory depends, at least in part, on its relative stability at sleep onset: Strong memories tend to be preserved, while weaker memories erode still further. An important aspect of memory consolidation may thus result from the removal of irrelevant memory “debris.

Internal Conversion of Valence-Shell Electrons : Measurement and Analysis for the 10.84 KeV Transition in 206Bi

開始ページ、終了ページ: 冊子体のページ付

Nonchiral Edge States at the Chiral Metal Insulator Transition in Disordered Quantum Hall Wires

The quantum phase diagram of disordered wires in a strong magnetic field is studied as a function of wire width and energy. The two-terminal conductance shows zero-temperature discontinuous transitions between exactly integer plateau values and zero. In the vicinity of this transition, the chiral metal-insulator transition (CMIT), states are identified that are superpositions of edge states with opposite chirality. The bulk contribution of such states is found to decrease with increasing wire width. Based on exact diagonalization results for the eigenstates and their participation ratios, we conclude that these states are characteristic for the CMIT, have the appearance of nonchiral edges states, and are thereby distinguishable from other states in the quantum Hall wire, namely, extended edge states, two-dimensionally (2D) localized, quasi-1D localized, and 2D critical states.Comment: replaced with revised versio

Stress acts cumulatively to precipitate Alzheimer’s disease-like tau pathology and cognitive deficits

Stressful life experiences are likely tiological factors in sporadic forms of Alzheimer’s disease (AD). Many AD patients hypersecrete glucocorticoids (GCs), and their GC levels correlate with the rate of cognitive impairment and extent of neuronal atrophy. Severity of cognitive deficits in AD correlates strongly with levels of perphosphorylated forms of the cytoskeletal protein TAU, an essential mediator of the actions of amyloid Beta (ABeta ), another molecule with a key pathogenic role in AD. Our objective was to investigate the sequential interrelationships between these various pathogenic elements, in particular with respect to the mechanisms through which stress might precipitate cognitive decline. We thus examined whether stress, through the mediation of GCs, influences TAU hyperphosphorylation, a critical and early event in the cascade of processes leading to AD pathology. Results from healthy, wild-type, middle-aged rats show that chronic stress and GC induce abnormal hyperphosphorylation of TAU in the hippocampus and prefrontal cortex (PFC), with contemporaneous impairments of hippocampus- and PFC-dependent behaviors. Exogenous GC potentiated the ability of centrally infused ABeta to induce hyperphosphorylation of TAU epitopes associated with AD and cytoplasmic accumulation of TAU, while previous exposure to stress aggravated the biochemical and behavioral effects of GC in ABeta-infused animals. Thus, lifetime stress/GC exposure may have a cumulative impact on the onset and progress of AD pathology, with TAU hyperphosphorylation serving to transduce the negative effects of stress and GC on cognition.Marie Curie Training FellowshipsEU CRESCENDO Consortium contract FP6-018652University College, London.Max Planck Society and European Union (EU) German-Portuguese Luso-Alemas Program and the EU CRESCENDO Consortium (Contract FP6-018652).German-Portuguese Luso-Alemas Progra

Instantons in N=1/2 Super Yang-Mills Theory via Deformed Super ADHM Construction

We study an extension of the ADHM construction to give deformed anti-self-dual (ASD) instantons in N=1/2 super Yang-Mills theory with U(n) gauge group. First we extend the exterior algebra on superspace to non(anti)commutative superspace and show that the N=1/2 super Yang-Mills theory can be reformulated in a geometrical way. By using this exterior algebra, we formulate a non(anti)commutative version of the super ADHM construction and show that the curvature two-form superfields obtained by our construction do satisfy the deformed ASD equations and thus we establish the deformed super ADHM construction. We also show that the known deformed U(2) one instanton solution is obtained by this construction.Comment: 32 pages, LaTeX, v2: typos corrected, references adde

Toxic tau oligomer formation blocked by capping of cysteine residues with 1,2-dihydroxybenzene groups

Neurofibrillary tangles, composed of hyperphosphorylated tau fibrils, are a pathological hallmark of Alzheimer's disease; the neurofibrillary tangle load correlates strongly with clinical progression of the disease. A growing body of evidence indicates that tau oligomer formation precedes the appearance of neurofibrillary tangles and contributes to neuronal loss. Here we show that tau oligomer formation can be inhibited by compounds whose chemical backbone includes 1,2-dihydroxybenzene. Specifically, we demonstrate that 1,2-dihydroxybenzene-containing compounds bind to and cap cysteine residues of tau and prevent its aggregation by hindering interactions between tau molecules. Further, we show that orally administered DL-isoproterenol, an adrenergic receptor agonist whose skeleton includes 1,2-dihydroxybenzene and which penetrates the brain, reduces the levels of detergent-insoluble tau, neuronal loss and reverses neurofibrillary tangle-associated brain dysfunction. Thus, compounds that target the cysteine residues of tau may prove useful in halting the progression of Alzheimer's disease and other tauopathies