| 1. |
- Andreasen, N, et al.
(författare)
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Cerebrospinal fluid tau and Abeta42 as predictors of development of Alzheimer's disease in patients with mild cognitive impairment
- 1999
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Ingår i: Neuroscience Letters. - 0304-3940. ; 273:1, s. 5-8
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Tidskriftsartikel (refereegranskat)abstract
- We studied CSF-tau and CSF-Abeta42 in 16 patients with mild cognitive impairment (MCI) who at follow-up investigations 6-27 months later had progressed to Alzheimer's disease (AD) with dementia. For comparison, we studied 15 age-matched healthy individuals. At baseline, 14/16 (88%) of MCI patients had high CSF-tau and/or low CSF-Abeta42 levels. These findings show that these CSF-markers are abnormal before the onset of clinical dementia and that they may help to identify MCI patients that will develop AD. This is especially important when drugs with potential effects on the progression of AD will reach the clinical phase.
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| 2. |
- Hornfelt, M., et al.
(författare)
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Upregulation of cytosolic phospholipase A2 correlates with apoptosis in mouse superior cervical and dorsal root ganglia neurons
- 1999
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Ingår i: Neuroscience Letters. - 0304-3940. ; 265:2, s. 87-90
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Tidskriftsartikel (refereegranskat)abstract
- The involvement of cytosolic phospholipase A2 (cPLA2) in apoptosis of adult mouse superior cervical and dorsal root ganglia neurons has been investigated by the use of immunohistochemistry for cPLA2 and DNA nick-end labeling for apoptotic cells, respectively, cPLA2 immunoreactivity was strongly upregulated in neurons of both preparations during in vitro culturing. By double labeling it was unequivocally demonstrated that cPLA2 was present and upregulated only in neurons undergoing apoptosis. A similar picture emerged when cPLA2 immunoreactivity was compared with staining with Fluoro-Jade, a novel fluorochrome marker for neuronal degeneration. The preferential presence of cPLA2 in apoptotic and degenerating cells suggests that the enzyme is important for some mechanism involved in or intimately coupled to neuronal cell death.
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| 3. |
- Minthon, Lennart, et al.
(författare)
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The apolipoprotein E epsilon4 allele frequency is normal in fronto-temporal dementia, but correlates with age at onset of disease
- 1997
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Ingår i: Neuroscience Letters. - 0304-3940. ; 226:1, s. 65-68
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Tidskriftsartikel (refereegranskat)abstract
- The apolipoprotein (apoE) epsilon4 allele was studied in fronto-temporal dementia (FTD), a diagnostic category including the specific disorders Pick's disease and frontal lobe degeneration of non-Alzheimer type (FLD). These dementing diseases have neuronal and synaptic degeneration in common with Alzheimer's disease (AD), for which the presence of the apoE epsilon4 allele is a known risk factor, and lowers the age of onset of disease. Previous studies on the apoE epsilon4 allele frequency in FTD have been inconclusive. The structural hallmarks of AD, allegedly linked to apoE presentation, neuritic plaques (NP), primarily composed of aggregates of beta-amyloid, and neurofibrillary tangles (NFT), primarily composed of hyperphosphorylated tau, are lacking in FTD. However, tau-positive cytoskeletal pathology is found in Pick's disease, but not in FLD. Resolving whether the epsilon4 frequency is increased in FTD or not may thus give clues to the pathogenetic mechanism of apoE in AD. We therefore studied apoE alleles in a well characterized material of FTD patients. The epsilon4 allele frequency was similar in 25 patients with FTD (14.0%) as compared with 26 healthy controls (13.5%). A post-mortem neuropathological examination was performed in 10 cases (nine had FLD and one Pick's disease). Our finding of a normal epsilon4 allele frequency in our group of FTD, principally consisting of FLD cases, support hypotheses involving differential binding of apoE to beta-amyloid and/or tau, in the development of beta-amyloid deposition and NP formation and/or tau hyperphosphorylation and NFT formation, for the pathogenetic role of apoE in AD. The age at onset was significantly lower (P < 0.01) in FTD patients possessing the epsilon4 allele (48.7 +/- 8.0 years) than in patients not possessing this allele (58.9 +/- 7.6 years). We conclude that, although the apoE epsilon4 allele frequency is not increase in FTD, the epsilon4 allele is not an etiological factor, but may rather be an accelerating factor in the degenerative process of FTD, thereby resulting in an earlier presentation of the disorder in individuals predisposed to develop FTD.
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| 4. |
- Perez, M T, et al.
(författare)
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Expression of brain-derived neurotrophic factor and of its functional receptor in neonatal and adult rat retina
- 1995
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Ingår i: Neuroscience Letters. - 0304-3940. ; 183:1-2, s. 9-96
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Tidskriftsartikel (refereegranskat)abstract
- The expression of mRNA coding for brain-derived neurotrophic factor (BDNF) and for its functional receptor, the full-length tyrosine kinase receptor trkB (trkB mRNA), was examined in early postnatal and adult rat retina by in situ hybridization using digoxygenin and radioactively-labeled oligonucleotide probes. BDNF and trkB mRNAs are expressed in the ganglion cell layer at postnatal-days (PN) 1, 4, 7, 14, 60, in proximal neuroblastic layer (PN 1, 4, 7), and proximal inner nuclear layer (PN 14, 60). Subpopulations of developing and mature retinal cells are thus capable of synthesizing BDNF.
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| 5. |
- Svensson, Bodil, et al.
(författare)
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Increased levels of mitogen activated protein kinase (MAP-K) detected in the injured adult mouse sciatic nerve
- 1995
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Ingår i: Neuroscience Letters. - 0304-3940. ; 200:1, s. 33-36
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Tidskriftsartikel (refereegranskat)abstract
- Adult mouse sciatic nerves (SNs) with attached dorsal root ganglia (DRG) were analysed for the presence of mitogen activated protein kinase (MAP-K) during normal and regenerative conditions. By immunohistochemistry, MAP-k was found to be present in the normal nerve at low levels in both Schwann cells and DRG nerve cell bodies, with a profoundly increased expression during regeneration. In axonal outgrowth assays, treatment with 2 mM 2-aminopurine (2-AP), a MAP-K antagonist, inhibited the regeneration of axons from the SN as well as from the cultured superior cervical ganglia. The reduced outgrowth was probably not due to toxic effects of the drug since the ganglionic protein synthesis was not inhibited. It is possible that 2-AP inteferes with regeneration-related events by inhibition of MAP-K.
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| 6. |
- Wang, Z Y, et al.
(författare)
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Electroconvulsive treatment evokes release of preprotachykinin-A mRNA into the cerebrospinal fluid and ocular aqueous humor of rabbits
- 1997
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Ingår i: Neuroscience Letters. - : Elsevier BV. - 0304-3940. ; 226:3, s. 151-154
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Tidskriftsartikel (refereegranskat)abstract
- Following electroconvulsive treatment (ECT) of rabbits, preprotachykinin-A (PPT-A) mRNA was detected by Southern blot analysis of polymerase chain reaction (PCR)-amplified products in the cerebrospinal fluid (CSF) and aqueous humor of the eye. In contrast, no PPT-A mRNA could be detected in samples from untreated animals. In addition, several neuropeptides (substance P, neuropeptide Y, cholecystokinin, calcitonin gene-related peptide and pituitary adenylate cyclase activating peptide) were released into the CSF (and aqueous humor) following ECT. The results suggest that PPT-A mRNA was released together with neuropeptides into the CSF and aqueous humor in response to ECT. Indeed, previous studies have suggested that neurons can release neuropeptide mRNAs and that neurons are capable of taking up and expressing foreign mRNA. If neuropeptide mRNA can be taken up and utilized by another neuronal population, it might explain instances when neurons display 'phenotypic switch', i.e. the transient expression of novel neuropeptides.
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| 7. |
- Wiklund, Peter, et al.
(författare)
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Protein kinase C inhibition has only a transient growth arresting effect on in vitro regenerating mouse sensory neurons
- 1999
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Ingår i: Neuroscience Letters. - 0304-3940. ; 275:3, s. 155-158
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Tidskriftsartikel (refereegranskat)abstract
- Adult mice sensory ganglia were cultured in an extracellular matrix gel. Analyses of extending axons were made 48 h (long-term) or immediately (short-term) after addition of protein kinase inhibitors. Long- and short-term growth was insensitive to protein kinase A/G inhibition by HA-1004. Long-term protein kinase C inhibition by chelerythrine affected only certain, long axons. In the short-term virtually all axon growth was arrested, but largely recovered on the following day. When combined, the drugs inhibited all long- and short-term growth and largely prevented the recovery of the latter. The transient effect by chelerythrine, and the permanent inhibition after combination with HA-1004, suggests compensatory mechanisms, perhaps via other kinases. Copyright (C) 1999 Elsevier Science Ireland Ltd.
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