|
Differential expression of galanin in the cholinergic basal forebrain of patients with Lewy body disorders.
Bottom Line:
Gallatin immunohistochemistry was carried out on anterior nbM sections from 76 LBD cases (27 PD, 15 PD with mild cognitive impairment (MCI), 34 PD with dementia (PDD) and 4 aged-matched controls.The LBD group had significantly higher galaninergic innervation scores (p = 0.016) compared to controls.However, this difference was due to increased innervation density only in a subgroup of LBD cases and this correlated positively with choline acetyltransferase-immunopositive neuron density.
View Article:
PubMed Central - PubMed
Affiliation: Division of Brain Sciences, Department of Medicine, Imperial College London, Burlington Danes Building, Hammersmith Hospital Campus, London, W12 0NN, UK. a.s.alexandris@gmail.com.
ABSTRACT
Show MeSH
Introduction: Depletion of cholinergic neurons within the nucleus basalis of Meynert (nbM) is thought to contribute to the development of cognitive impairments in both Alzheimer's disease (AD) and Lewy body disorders (LBD). It has been reported that, in late stage AD, a network of fibres that contain the neuropeptide galanin displays significant hypertrophy and 'hyperinnervates' the surviving cholinergic neurons. Galanin is considered as a highly inducible neuroprotective factor and in AD this is assumed to be part of a protective tissue response. The aim of this study was to determine if a similar galanin upregulation is present in the nbM in post-mortem tissue from patients with LBD. Gallatin immunohistochemistry was carried out on anterior nbM sections from 76 LBD cases (27 PD, 15 PD with mild cognitive impairment (MCI), 34 PD with dementia (PDD) and 4 aged-matched controls. Galaninergic innervation of cholinergic neurons was assessed on a semi-quantitative scale. Results: The LBD group had significantly higher galaninergic innervation scores (p = 0.016) compared to controls. However, this difference was due to increased innervation density only in a subgroup of LBD cases and this correlated positively with choline acetyltransferase-immunopositive neuron density. Conclusion: Galanin upregulation within the basal forebrain cholinergic system in LBD, similar to that seen in AD, may represent an intrinsic adaptive response to neurodegeneration that is consistent with its proposed roles in neurogenesis and neuroprotection. Related in: MedlinePlus |
Related In:
Results -
Collection
License 1 - License 2 getmorefigures.php?uid=PMC4666186&req=5
Fig4: Galanin like immunoreactivity (GAL-ir) of putative cholinergic neurons. a-b Sections of ChAT (a) and galanin (b) immunostaining of the nucleus basalis magnocellular neurons from the same case; * denotes same anatomical landmark. c Example of minimal somal immunoreactity. d Example of intense perikaryal GAL-ir. e-f Galaninergic innervation of putative cholinergic neurons (arrow heads) Mentions: Intense somal GAL-ir was observed in the hypothalamic nuclei (Fig. 3a-b) and the supraoptic nucleus (SON) exhibited variable levels of perikaryal staining and very few fibres (Fig. 3c-d). Some somal GAL-ir was observed in the nbM and sections from the same case immunostained with galanin and ChAT antibodies reveal immunoreactivity of the same magnocellular cell population (Fig. 4a-b). It was noticed that there was no concordance between perikaryal staining intensity in the SON and that of the neighbouring nbM neurons. Confocal microscopy demonstrated low level galanin immunofluorescence in both SON and nbM magnocellular neurons (Fig. 5a-b).Fig. 4 |
View Article: PubMed Central - PubMed
Affiliation: Division of Brain Sciences, Department of Medicine, Imperial College London, Burlington Danes Building, Hammersmith Hospital Campus, London, W12 0NN, UK. a.s.alexandris@gmail.com.
Introduction: Depletion of cholinergic neurons within the nucleus basalis of Meynert (nbM) is thought to contribute to the development of cognitive impairments in both Alzheimer's disease (AD) and Lewy body disorders (LBD). It has been reported that, in late stage AD, a network of fibres that contain the neuropeptide galanin displays significant hypertrophy and 'hyperinnervates' the surviving cholinergic neurons. Galanin is considered as a highly inducible neuroprotective factor and in AD this is assumed to be part of a protective tissue response. The aim of this study was to determine if a similar galanin upregulation is present in the nbM in post-mortem tissue from patients with LBD. Gallatin immunohistochemistry was carried out on anterior nbM sections from 76 LBD cases (27 PD, 15 PD with mild cognitive impairment (MCI), 34 PD with dementia (PDD) and 4 aged-matched controls. Galaninergic innervation of cholinergic neurons was assessed on a semi-quantitative scale.
Results: The LBD group had significantly higher galaninergic innervation scores (p = 0.016) compared to controls. However, this difference was due to increased innervation density only in a subgroup of LBD cases and this correlated positively with choline acetyltransferase-immunopositive neuron density.
Conclusion: Galanin upregulation within the basal forebrain cholinergic system in LBD, similar to that seen in AD, may represent an intrinsic adaptive response to neurodegeneration that is consistent with its proposed roles in neurogenesis and neuroprotection.
