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Sökning: L773:1534 6293 OR L773:1528 4042

  • Resultat 1-14 av 14
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  • Aarsland, D, et al. (författare)
  • Mild cognitive impairment in Parkinson's disease
  • 2011
  • Ingår i: Current neurology and neuroscience reports. - : Springer Science and Business Media LLC. - 1534-6293 .- 1528-4042. ; 11:4, s. 371-378
  • Tidskriftsartikel (refereegranskat)
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  • Ballard, C, et al. (författare)
  • Psychosis in Alzheimer's Disease
  • 2020
  • Ingår i: Current neurology and neuroscience reports. - : Springer Science and Business Media LLC. - 1534-6293 .- 1528-4042. ; 20:12, s. 57-
  • Tidskriftsartikel (refereegranskat)abstract
    • Purpose of ReviewTo review the incidence, treatment and genetics of psychosis in people with mild cognitive impairment (MCI) and Alzheimer’s disease (AD).Recent FindingsPsychosis in Alzheimer’s disease (AD) has an incidence of ~ 10% per year. There is limited evidence regarding psychological interventions. Pharmacological management has focused on atypical antipsychotics, balancing modest benefits with evidence of long-term harms. The 5HT2A inverse agonist pimavanserin appears to confer benefit in PD psychosis with initial evidence of benefit in AD. Cholinesterase inhibitors give modest benefits in DLB psychosis. The utility of muscarinic agonists, lithium, glutamatergic and noradrenergic modulators needs further study.SummaryRecent work has confirmed the importance of psychosis in MCI as well as AD. The lack of evidence regarding psychological therapies is an urgent knowledge gap, but there is encouraging evidence for emerging pharmacological treatments. Genetics will provide an opportunity for precision medicine and new treatment targets.
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  • Engström, Maria, et al. (författare)
  • Neuroimaging in the Kleine-Levin Syndrome
  • 2018
  • Ingår i: Current Neurology and Neuroscience Reports. - Philadelphia, United States : Springer Science and Business Media LLC. - 1528-4042 .- 1534-6293. ; 18:9
  • Forskningsöversikt (refereegranskat)abstract
    • PURPOSE OF REVIEW: The purpose was to review the most recent literature on neuroimaging in the Kleine-Levin syndrome (KLS). We aimed to investigate if frontotemporal and thalamic dysfunction are key KLS signatures, and if recent research indicates other brain networks of interest that elucidate KLS symptomatology and aetiology.RECENT FINDINGS: In a comprehensive literature search, we found 12 original articles published 2013-2018. Most studies report deviations related to cerebral perfusion, glucose metabolism, or blood-oxygen-level-dependent responses in frontotemporal areas and/or the thalamus. Studies also report dysfunction in the temporoparietal junction and the oculomotor network that also were related to clinical parameters. We discuss these findings based on recent research on thalamocortical networks and brain stem white matter tracts. The hypothesis of frontotemporal and thalamic involvement in KLS was confirmed, and additional findings in the temporoparietal junction and the oculomotor system suggest a broader network involvement, which can be investigated by future high-resolution and multimodal imaging.
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  • Jóhannesson, Gauti, 1979-, et al. (författare)
  • Intracranial and Intraocular Pressure at the Lamina Cribrosa : Gradient Effects
  • 2018
  • Ingår i: Current Neurology and Neuroscience Reports. - : Springer. - 1528-4042 .- 1534-6293. ; 18:5
  • Forskningsöversikt (refereegranskat)abstract
    • Purpose of Review: A pressure difference between the intraocular and intracranial compartments at the site of the lamina cribrosa has been hypothesized to have a pathophysiological role in several optic nerve head diseases. This paper reviews the current literature on the translamina cribrosa pressure difference (TLCPD), the associated pressure gradient, and its potential pathophysiological role, as well as the methodology to assess TLCPD.Recent Findings: For normal-tension glaucoma (NTG), initial studies indicated low intracranial pressure (ICP) while recent findings indicate that a reduced ICP is not mandatory.Summary: Data from studies on the elevated TLCPD as a pathophysiological factor of NTG are equivocal. From the identification of potential postural effects on the cerebrospinal fluid (CSF) communication between the intracranial and retrolaminar space, we hypothesize that the missing link could be a dysfunction of an occlusion mechanism of the optic nerve sheath around the optic nerve. In upright posture, this could cause an elevated TLCPD even with normal ICP and we suggest that this should be investigated as a pathophysiological component in NTG patients.
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  • Puschmann, Andreas (författare)
  • New Genes Causing Hereditary Parkinson’s Disease or Parkinsonism
  • 2017
  • Ingår i: Current Neurology and Neuroscience Reports. - : Springer Science and Business Media LLC. - 1528-4042 .- 1534-6293. ; 17, s. 1-11
  • Forskningsöversikt (refereegranskat)abstract
    • Purpose of Review: This article reviews was to review genes where putative or confirmed pathogenic mutations causing Parkinson’s disease or Parkinsonism have been identified since 2012, and summarizes the clinical and pathological picture of the associated disease subtypes. Recent Findings: Newly reported genes for dominant Parkinson’s disease are DNAJC13, CHCHD2, and TMEM230. However, the evidence for a disease-causing role is not conclusive, and further genetic and functional studies are warranted. RIC3 mutations have been reported from one family but not yet encountered in other patients. New genes for autosomal recessive disease include SYNJ1, DNAJC6, VPS13C, and PTRHD1. Deletions of a region on chromosome 22 (22q11.2del) are also associated with early-onset PD, but the mode of inheritance and the underlying causative gene remain unclear. PODXL mutations were reported in autosomal recessive PD, but their roles remain to be confirmed. Mutations in RAB39B cause an X-linked Parkinsonian disorder. Summary: Mutations in the new dominant PD genes have generally been found in medium- to late-onset Parkinson’s disease. Many mutations in the new recessive and X-chromosomal genes cause severe atypical juvenile Parkinsonism, but less devastating mutations in these genes may cause PD.
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  • Velayudhan, L, et al. (författare)
  • New Therapeutic Strategies for Lewy Body Dementias
  • 2017
  • Ingår i: Current neurology and neuroscience reports. - : Springer Science and Business Media LLC. - 1534-6293 .- 1528-4042. ; 17:9, s. 68-
  • Tidskriftsartikel (refereegranskat)
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  • Xu, ZY, et al. (författare)
  • Paroxysmal Movement Disorders: Recent Advances
  • 2019
  • Ingår i: Current neurology and neuroscience reports. - : Springer Science and Business Media LLC. - 1534-6293 .- 1528-4042. ; 19:7, s. 48-
  • Tidskriftsartikel (refereegranskat)
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  • Resultat 1-14 av 14

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