Diffusive Propagation of Exciton-Polaritons through Thin Crystal Slabs.

If light beam propagates through matter containing point impurity centers, the amount of energy absorbed by the media is expected to be either independent of the impurity concentration N or proportional to N, corresponding to the intrinsic absorption or impurity absorption, respectively. Comparative studies of the resonant transmission of light in the vicinity of exciton resonances measured for 15 few-micron GaAs crystal slabs with different values of N, reveal a surprising tendency. While N spans almost five decimal orders of magnitude, the normalized spectrally-integrated absorption of light scales with the impurity concentration as N(1/6).

Suris tetrons: possible spectroscopic evidence for four-particle optical excitations of a two-dimensional electron gas.

The excitations of a two-dimensional electron gas in quantum wells with intermediate carrier density (ne∼1011  cm-2), i.e., between the exciton-trion and the Fermi-sea range, are so far poorly understood.

Amyloid-beta, tau protein, and oxidative changes as a physiological compensatory mechanism to maintain CNS plasticity under Alzheimer's disease and other neurodegenerative conditions.

In this review, we propose that the neurodegenerative changes in the neurochemistry of amyloid-beta (Abeta) aggregation, tau phosphorylation, cytoskeleton rearrangement, oxidative stress, and lipid peroxidation in Alzheimer's disease (AD), and a number of other neurodegenerative diseases, are secondary pathological features. In fact, we believe that these phenomena represent natural compensatory mechanisms for impaired primary neurodegeneration, membrane dynamic deterioration, and/or associated failures of neurotransmission, synaptic function, and neuroplasticity. Physiologically, Abeta, lipid peroxidation, and tau protein may function to sense changes in activity-dependent membrane properties and therefore biochemically modulate membrane lipid homeostasis for more efficient synaptic action.

Exciton spin decay modified by strong electron-hole exchange interaction.

We study exciton spin decay in the regime of strong electron-hole exchange interaction, which occurs in a wide variety of semiconductor nanostructures. In this regime the electron spin precession is restricted within a sector formed by the external magnetic field and the effective exchange fields triggered by random spin flips of the hole. Using Hanle effect measurements, we demonstrate that this mechanism dominates our experiments in CdTe/(Cd,Mg)Te quantum wells.

Direct detection of brain acetylcholine synthesis by magnetic resonance spectroscopy.

The cholinergic system is an important modulatory neurotransmitter system in the brain. Changes in acetylcholine concentration have been previously determined directly in animal models and human brain biopsy specimens, and indirectly, by the effects of drugs, in living humans. Here, we developed a method for direct determination of acetylcholine synthesis in living brain tissue.

Cholesterol homeostasis failure as a unifying cause of synaptic degeneration.

We previously showed that fine tuning of neural cholesterol dynamics is essential for basic synapse function, plasticity and behavior. Significant experimental evidence indicates that cholinergic function, ionotropic and metabotropic receptor machinery, excessive tau phosphorylation, the change of amyloid beta (Abeta or Abeta) biochemistry, neural oxidative stress reactions, and other features of neurodegeneration also depend on fine tuning of brain cholesterol homeostasis. This evidence suggest that (i) cholesterol homeostasis break is the unifying primary cause of sporadic and familial Alzheimer's disease (AD), neuromuscular diseases (particularly inclusion-body myositis), Niemann-Pick's type C disease and Down syndrome, and (ii) explains the overlap of neurodegenerative hallmarks across the spectrum of neurodegenerative diseases.

Amyloid-beta induced cell death is independent of free radicals.

Acutely dissociated rat cerebellar granule cell neurons were incubated with amyloid-beta (1-42) and studied by flow cytometry. Amyloid-beta caused a dose-dependent loss of viability, as determined by intracellular accumulation of propidium iodide (PI),and that was not accompanied by significant elevation of intracellular calcium, measured by Fluo-3 or reactive oxygen species (ROS), measured by 2',7'-dihydro-dichlorfluorescein diacetate (DCF). Carnosine, a ROS scavenger and an inhibitor of non-enzymatic glycosylation, partially reduced cell death caused by amyloid-beta.

Alzheimer's amyloid-beta (A beta) is an essential synaptic protein, not neurotoxic junk.

Despite a decade long universal publication in favor of the view on amyloid-beta (A beta) as Alzheimer's disease culprit (solely neurotoxic for neurons and brain tissue), current scientific evidence leaves little doubt that A beta serves an essential role at synapse and in synaptic structure-functional plasticity that underlie learning and memory. Therefore, the change of A beta biology in Alzheimer's disease (as well as in a number of other human pathologies, including cardiovascular disease, neuromuscular junction disorders, NPC and Down's syndrome) may represent a physiological mechanism to compensate for impaired brain structure or function. In our own recent study A beta 1-40 rescued long term potentiation (LTP, a major model for activity-dependent CNS plasticity), while cholesterol synthesis inhibition abolished the restorative action of the A beta peptide.

Brain cholesterol, statins and Alzheimer's Disease.

Growing evidence suggests that cellular cholesterol homeostasis is causally involved in different steps leading to pathological events in the brain of Alzheimer's Disease (AD) patients. It was previously demonstrated that the processing of the amyloid beta-peptide precursor protein (APP) is modulated by pronounced alterations in cellular cholesterol levels using statins or cholesterol extracting agents. However, a cholesterol-rich diet was found to enhance amyloid beta-peptide (Abeta) burden in the brain of transgenic mice without clearly affecting total brain cholesterol levels.

Cholesterol, synaptic function and Alzheimer's disease.

We experimentally modeled neuronal cholesterol imbalance by creating an acute biochemical increase in cholesterol turnover in rat hippocampal slices. This kind of experimental set-up impairs the redistribution of cholesterol from one cell to another via lipoprotein transport. While increasing cholesterol removal or immediately afterwards, we evoked and recorded two brain waveforms, paired pulse facilitation (PPF) and long-term potentiation (LTP), which indicate neurotransmission and synaptic plasticity, respectively.

Choline in the aging brain.

Proton magnetic resonance spectroscopy has been increasingly utilized in brain research to monitor non-invasively metabolites such as N-acetyl aspartate (NAA), creatine (Cr) and choline (Cho). We present here studies of the effect of aging on the ratios of these metabolites measured in the rat brain in vivo and on choline transport and lipid synthesis in rat brain slices, in vitro. The in vivo studies indicated that the ratios of Cho/NAA and Cho/Cr increased in the aged hippocampus, whereas the ratio of Cr/NAA was similar in the aged and adult hippocampus.

The levels of soluble amyloid beta in different high density lipoprotein subfractions distinguish Alzheimer's and normal aging cerebrospinal fluid: implication for brain cholesterol pathology?

Several previous studies reported the association of the soluble form of amyloid beta (sA beta) protein, a major constituent of amyloid deposits in Alzheimer's disease (AD), with normal blood, cerebrospinal fluid (CSF) and central nervous system high density lipoproteins (HDLs). The present report aimed to elucidate the pattern of sA beta and apolipoprotein (apo) distribution in AD CSF-HDL subfractions. We studied AD CSF-HDL subfractions by SDS/PAGE and immunoblot analysis after CSF fractionation via density flotation ultracentrifugation.

Alzheimer's Abeta1-40 peptide modulates lipid synthesis in neuronal cultures and intact rat fetal brain under normoxic and oxidative stress conditions.

The effect of amyloid beta (Abeta), the major constituent of the Alzheimer's (AD) brain on lipid metabolism was investigated in cultured nerve cells and in a fetal rat brain model. Differentiated (NGF) and undifferentiated PC12 cells or primary cerebral cell cultures were incubated with [14C]acetate in the absence or presence of Abeta1-40. Incorporation of label into lipid species was determined after lipid extraction and TLC separation.

Unilateral GluR2(B) hippocampal knockdown: a novel partial seizure model in the developing rat.

Kainic acid (KA) induces status epilepticus in both adult and young rats but with different consequences on pathology and gene expression. In adults, GluR2(B) AMPA subunit expression is markedly reduced in CA3 neurons before neurodegeneration. In pups, the GluR2(B) subunit is sustained, possibly contributing to neuronal survival.

Beta-amyloid: Alzheimer's disease and brain beta-amyloidoses.

This review considers some aspects of the biochemistry of beta-amyloid, a protein which produces insoluble deposits in the brain. These deposits are a specific morphological feature of Alzheimer's disease, Down's syndrome, and senile dementia. Our contribution to the concept of a soluble form of beta-amyloid as of a normal human protein is presented.

Biochemical assay for amyloid beta deposits to distinguish Alzheimer's disease from other dementias.

Biochemical markers for Alzheimer's disease (AD) are of great value for precise diagnosis and in studies of the pathogenetic processes of this disease. A new biochemical assay allowing to differentiate AD from other forms of dementia is described. The assay is based on the extraction of amyloid beta (A beta) from milligram amounts of brain tissue by using 20% acetonitrile in 0.

Alzheimer's amyloid beta interaction with normal human plasma high density lipoprotein: association with apolipoprotein and lipids.

We report studies of the interaction of Alzheimer's amyloid beta protein (A beta) with normal human plasma high density lipoprotein (HDL), aiming to clarify to which lipoprotein (LP) structural constituent (apolipoprotein or lipid) soluble A beta is primarily bound. Purified HDLs were incubated with biotinylated A beta 1-40 followed by LP repurification by size exclusion (SE) HPLC. SDS-PAGE, immunoblot and N-terminal sequence analysis of the biotin-A beta positive protein bands revealed that A beta is bound to many apolipoproteins of the HDL, mainly apoA-I, apoA-II, apoE and apoJ.

Alzheimer's soluble amyloid beta protein is secreted by HepG2 cells as an apolipoprotein.

Recently we reported that the soluble form of amyloid beta protein (sA beta) in normal human plasma and cerebrospinal fluid is associated with lipoprotein (LP) particles. In this paper we tested the sA beta secretion by cells in association with LP in the model of the human hepatoma HepG2 cell line. These cells secreted sA beta to the culture media and expressed intracellular sA beta immunoreactivity.