title: Differential expression of galanin in the cholinergic basal forebrain of patients with Lewy body disorders.
abstract: BACKGROUND
  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.
  
  
  CONCLUSIONS
  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.
authors.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.|School of Medicine, University of Leicester, Leicester, UK. a.s.alexandris@gmail.com.
authors.forename: Athanasios
authors.initials: A
authors.lastname: Alexandris
authors.affiliation: Division of Brain Sciences, Department of Medicine, Imperial College London, Burlington Danes Building, Hammersmith Hospital Campus, London, W12 0NN, UK.|Laboratory of Neurodegenerative Diseases, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR.
authors.forename: Alan King Lun
authors.initials: AK
authors.lastname: Liu
authors.affiliation: Laboratory of Neurodegenerative Diseases, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR.|Research Centre of Heart, Brain, Hormone, and Healthy Aging, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR.|State Key Laboratory of Brain and Cognitive Sciences, The University of Hong Kong, Pokfulam, Hong Kong SAR.
authors.forename: Raymond Chuen-Chung
authors.initials: RC
authors.lastname: Chang
authors.affiliation: Division of Brain Sciences, Department of Medicine, Imperial College London, Burlington Danes Building, Hammersmith Hospital Campus, London, W12 0NN, UK.
authors.forename: Ronald K B
authors.initials: RK
authors.lastname: Pearce
authors.affiliation: Division of Brain Sciences, Department of Medicine, Imperial College London, Burlington Danes Building, Hammersmith Hospital Campus, London, W12 0NN, UK. s.gentleman@imperial.ac.uk.
authors.forename: Steve M
authors.initials: SM
authors.lastname: Gentleman
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D018678:Cholinergic Agents / Q000378:metabolism*; D060825:Cognitive Dysfunction / Q000473:pathology; D015331:Cohort Studies; D005260:Female; D019004:Galanin / Q000378:metabolism*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D020961:Lewy Body Disease / Q000473:pathology*; D008297:Male; D018613:Microscopy, Confocal; D016548:Prosencephalon / Q000378:metabolism*; D018709:Statistics, Nonparametric
chemical_list: D018678:Cholinergic Agents; D005904:Glial Fibrillary Acidic Protein; D019004:Galanin