Neurobiology of Disease
Papers 4800
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#1Jinxu Liu (Creighton University)H-Index: 4
#2Gajanan P. Shelkar (Creighton University)H-Index: 8
Last.Shashank M. Dravid (Creighton University)H-Index: 19
view all 9 authors...
Abstract Impaired behavioral flexibility and repetitive behavior is a common phenotype in autism and other neuropsychiatric disorders, but the underlying synaptic mechanisms are poorly understood. The trans-synaptic glutamate delta (GluD)-Cerebellin 1-Neurexin complex, critical for synapse formation/maintenance, represents a vulnerable axis for neuropsychiatric diseases. We have previously found that GluD1 deletion results in reversal learning deficit and repetitive behavior. In this study, we s...
#1Jessica M. Livingston (U of O: University of Ottawa)
#2Matthew W. McDonald (U of O: University of Ottawa)H-Index: 8
Last.Dale Corbett (U of O: University of Ottawa)H-Index: 50
view all 10 authors...
Abstract Vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH) and memory deficits, and often occurs concurrently with metabolic syndrome (MetS). Despite their common occurrence, it is unknown whether CCH and MetS act synergistically to exacerbate VCI-associated pathology. Here, using male Sprague-Dawley rats, we examined the effects of a clinically relevant model of adolescent-onset MetS and adult-onset CCH on neuro-vascular outcomes, combining a cafeteria ...
#1Tomohiro Imamura (Kyushu University)H-Index: 2
#2Yuki T. Yanagihara (Kyushu University)H-Index: 2
Last.Jun-ichi Kira (Kyushu University)H-Index: 54
view all 11 authors...
Abstract The toxic conformer of amyloid β-protein (Aβ) ending at 42 (Aβ42), which contains a unique turn conformation at amino acid residue positions 22 and 23 and tends to form oligomers that are neurotoxic, was reported to play a critical role in the pathomechanisms of Alzheimer's disease (AD), in which diabetes mellitus (DM)-like mechanisms are also suggested to be operative. It remains to be established whether the attenuation of insulin signaling is involved in an increase of toxic Aβ42 con...
#1Magdalena K. Baaske (University of Lübeck)
#2Edgar R. Kramer (Plymouth University)H-Index: 20
Last.Christian K.E. Moll (UHH: University of Hamburg)H-Index: 14
view all 6 authors...
Abstract Loss-of-function mutations in the parkin-encoding PARK2 gene are a frequent cause of young-onset, autosomal recessive Parkinson's disease (PD). Parkin knockout mice have no nigro-striatal neuronal loss but exhibit abnormalities of striatal dopamine transmission and cortico-striatal synaptic function. How these predegenerative changes observed in vitro affect neural dynamics at the intact circuit level, however, remains hitherto elusive. Here, we recorded from motor cortex, striatum and ...
#1Aaron D. Schwab (UNMC: University of Nebraska Medical Center)
#2Mackenzie J. Thurston (UNMC: University of Nebraska Medical Center)
Last.R Lee Mosley (UNMC: University of Nebraska Medical Center)H-Index: 41
view all 7 authors...
Abstract With the increasing prevalence of Parkinson’s disease (PD), there is an immediate need to interdict disease signs and symptoms. In recent years this need was met through therapeutic approaches focused on regenerative stem cell replacement and alpha-synuclein clearance. However, neither have shown long-term clinical benefit. A novel therapeutic approach designed to affect disease is focused on transforming the brain’s immune microenvironment. As disordered innate and adaptive immune func...
Abstract Exposure of mouse mixed cortical cell cultures to lipopolysaccharide (LPS) resulted in inflammasome formation in neurons and astrocytes, as indicated by increases in the levels of NLRP3, ASC, caspase-1, and IL-1β. LPS exposure concurrently increased the level of free zinc in the cytosol of both cell types. Addition of the membrane-permeant zinc chelator TPEN blocked the increases in the levels of NLRP3 and caspase-1 as well as the release of inflammatory cytokines, indicating a role for...
#1Michele Iacomino (UniGe: University of Genoa)H-Index: 6
#2Roberto DolianaH-Index: 23
Last.Paola Lanteri (Istituto Giannina Gaslini)H-Index: 4
view all 24 authors...
Abstract Elastin microfibril interface-located proteins (EMILINs) are extracellular matrix glycoproteins implicated in elastogenesis and cell proliferation. Recently, a missense mutation in the EMILIN1 gene has been associated with autosomal dominant connective tissue disorder and motor-sensory neuropathy in a single family. We identified by whole exome sequencing a novel heterozygous EMILIN1 mutation c.748C>T [p.R250C] located in the coiled coil forming region of the protein, in four affected m...
#1Heather Hulme (Uppsala University)
#2Elva Fridjonsdottir (Uppsala University)H-Index: 1
Last.Per E. Andrén (Uppsala University)H-Index: 36
view all 11 authors...
Abstract Neuropeptides are important signalling molecules in the brain and alterations in their expression levels have been linked to neurological disorders such as Parkinson's disease. It is challenging to map neuropeptide changes across and within brain regions because of their low in vivo concentrations and complex post-translational processing. Consequently, the role of neuropeptides in Parkinson's disease is not well understood. Thus, we have developed and validated a method to image multip...
Abstract Spontaneous, recurrent spreading depolarizations (SD) are increasingly more appreciated as a pathomechanism behind ischemic brain injuries. Although the prostaglandin F2α - FP receptor signaling pathway has been proposed to contribute to neurodegeneration, it has remained unexplored whether FP receptors are implicated in SD or the coupled cerebral blood flow (CBF) response. We set out here to test the hypothesis that FP receptor blockade may achieve neuroprotection by the inhibition of ...
#1Elizabeth M. Rhea (UW: University of Washington)H-Index: 7
#2Jacob Raber (OHSU: Oregon Health & Science University)H-Index: 45
Last.William A. Banks (UW: University of Washington)H-Index: 93
view all 3 authors...
Abstract Central nervous system (CNS) insulin resistance is associated with Alzheimer's disease (AD). In addition, the apolipoprotein E4 (apoE4) isoform is a risk factor for AD. The connection between these two factors in relation to AD is being actively explored. We summarize this literature with a focus on the transport of insulin and apoE across the blood-brain barrier (BBB) and into the CNS, the impact of apoE and insulin on the BBB, and the interactions between apoE, insulin, and the insuli...
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Molecular biology