New biomarkers are needed to improve knowledge about pathophysiology, in order to provide earlier correct diagnosis and to follow disease progression of the neurodegenerative diseases amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD). The aim of this thesis was to find new biomarkers for these diseases. First, increased serum levels and unchanged levels in postmortal spinal cord of vascular endothelial growth factor (VEGF) were demonstrated. VEGF was not detected in cerebrospinal fluid (CSF) in ALS. Second, increased levels of fibroblast growth factor 2 were found in the CSF and serum of ALS patients. Both studies used enzyme-linked immunoassays. Third, a proteomics method for CSF analysis was explored, based on tryptic digestion and subsequent separation and detection of the peptides by on-line liquid chromatography-Fourier transform ion cyclotron resonance mass spectrometry. ALS-specific patterns were observed. Four out of five samples were correctly assigned, but no single protein biomarker could be identified. Fourth, [11C](L)-deprenyl-D2 (DED) positron emission tomography (PET) demonstrated increased retention in the pons and white matter in ALS. DED binds to monoamino oxidase B, which in the brain is primarily located in astrocytes. Thus evidence was provided that astrocytosis may be detected in vivo in ALS. Fifth, normal [11C]-PIB binding in five nondemented patients with PD was reported, in contrast to previous findings of increased retention in Alzheimer's disease reflecting amyloid aggregation. Finally, the combined use of fluorodeoxyglucose and L-[β 11C]-DOPA PET for the differential diagnosis of parkinsonian syndromes was evaluated. PET provided support for the clinical diagnosis in 62 out of 75 patients, and served to exclude suspected diagnoses in another five patients.

BACKGROUND: Idiopathic normal pressure hydrocephalus (INPH) is still a syndrome generating more questions than answers. Today, research focuses mainly on two areas: understanding the pathophysiology – especially how the malfunctioning CSF system affects the brain parenchyma – and finding better methods to select patients benefiting from a shunt operation. This thesis targets the aspect of finding better selection methods by investigating the measurability of intracranial pressure via lumbar space, and determining if intraparenchymal measurement of long-term ICP-oscillations (B-waves) could be replaced by short-term measurements of CSF pulse pressure waves via lumbar space. Furthermore, I look into the interaction between the CSF system and the parenchyma itself by investigating how the cortical activity of the brain changes after long-term CSF drainage, and if there is any regress in the suggested ischemia after this intervention. Finally, I examine if the neuronal integrity in the INPH brain is impaired, and if this feature is relevant for the likeliness of improvement after CSF diversion. METHODS: The comparison of intracranial and lumbar pressure was made over a vast pressure interval using our unique CSF infusion technique, and it included ten INPH patients. Pressure was measured via lumbar space and in brain tissue, and the pressures were compared using a general linear model. Short-term lumbar pressure waves were quantified by determining the slope between CSF pulse pressure and mean pressure, defined as the relative pulse pressure coefficient (RPPC). The correlation between RPPC, B-waves and CSF outflow resistance was investigated. In a prospective study, functional MRI was used to assess brain activity before and after long-term CSF drainage of 400 ml of CSF in eleven INPH patients. The functionalities tested included finger movement, memory, and attention. The results were benchmarked against the activity in ten healthy controls to identify the brain areas improving after drainage. The ischemia (Lactate) and neuronal integrity (NAA and Choline) were measured in a similar manner in 16 patients using proton MR spectroscopy, and the improvement of the patients after CSF drainage was based on assessment of their gait. RESULTS: There was excellent agreement between ICP measured in brain tissue and via lumbar space (regression coefficient = 0.98, absolute difference < 1 mm Hg). Adjusting for the separation distance between the measuring devices slightly worsened the agreement, indicating other factors influencing the measured difference as well. RPPC measured via lumbar space significantly correlated to the presence of B-waves, but not to outflow resistance. In the prospective study, controls outperformed patients on clinical tests as well as tasks related to the experiments. Improved behaviour after CSF drainage was found for motor function only, and it was accompanied by increased activation in the supplementary motor area (SMA). No lactate was detected, either before or after CSF drainage. NAA was decreased in INPH patients compared to controls, and the NAA levels were higher in the patients improving after drainage. CONCLUSIONS: ICP can be accurately measured via lumbar space in patients with communicating CSF systems. The close relation between RPPC and B-waves indicates that B-waves are primarily related to intracranial compliance, and that measurement of RPPC via lumbar space could possibly substitute B-wave assessment as selection method for finding suitable patients for shunt surgery. Improvement in motor function after CSF drainage was associated to enhanced activity in SMA, supporting the involvement of the cortico-basal ganglia-thalamo-cortical loop in the pathophysiology of INPH. There was no evidence indicating a widespread low-graded ischemia in INPH; however, there was a neuronal dysfunction in frontal white matter as indicated by the reduced levels of NAA. In addition, the level of neuronal dysfunction was related to the likeliness of improvement after CSF removal, normal levels of NAA predisposing for recovery.

Peripheral nerve trauma is a common cause of considerable functional morbidity, and healthcare expenditure. Particularly in the ~15% of injuries unsuitable for primary repair, standard clinical management results in inadequate sensory restitution in the majority of cases, despite the rigorous application of complex microsurgical techniques. This can largely be explained by the failure of surgical management to adequately address the neurobiological hurdles to optimal regeneration. Most significant of these is the extensive sensory neuronal death that follows injury, and which is accompanied by a reduction in the regenerative potential of axotomised neurons, and in the supportive capacity of the Schwann cell population if nerve repair is delayed. The present study aimed to accurately delineate the timecourse of neuronal death, in order to identify a therapeutic window during which clinically applicable neuroprotective strategies might be adopted. It then proceeded to investigate means to increase the regenerative capacity of chronically axotomised neurons, and to augment the Schwann cells’ ability to promote that regenerative effort. Unilateral sciatic nerve transection in the rat was the model used, initially assessing neuronal death within the L4&amp;5 dorsal root ganglia by a combination of morphology, TdT uptake nick-end labelling (TUNEL), and statistically unbiased estimation of neuronal loss using the stereological optical disector technique. Having identified 2 weeks, and 2 months post-axotomy as the most biologically relevant timepoints to study, the effect upon neuronal death of systemic treatment with acetyl-L-carnitine (ALCAR 10, or 50mg/kg/day) or N-acetyl-cysteine (NAC 30, or 150mg/kg/day) was determined. A model of secondary nerve repair was then adopted; either 2 or 4 months after unilateral sciatic nerve division, 1cm gap repairs were performed using either reversed isografts, or poly-3-hydroxybutyrate (PHB) conduits containing an alginate-fibronectin hydrogel. Six weeks later nerve regeneration and the Schwann cell population were quantified by digital image analysis of frozen section immunohistochemistry. Sensory neuronal death begins within 24 hours of injury, but takes 1 week to translate into significant neuronal loss. The rate of neuronal death peaks 2 weeks after injury, and neuronal loss is essentially complete by 2 months post-axotomy. Nerve repair is incompletely neuroprotective, but the earlier it is performed the greater the benefit. Two clinically safe pharmaceutical agents, ALCAR &amp; NAC, were found to virtually eliminate sensory neuronal death after peripheral nerve transection. ALCAR also enhanced nerve regeneration independently of its neuroprotective role. Plain PHB conduits were found to be technically simple to use, and supported some regeneration, but were not adequate in themselves. Leukaemia inhibitory factor enhanced nerve regeneration, though cultured autologous Schwann cells (SC’s) were somewhat more effective. Both were relatively more efficacious after a 4 month delay in nerve repair. The most profuse regeneration was found with recombinant glial growth factor (rhGGF-2) in repairs performed 2 months after axotomy, with results that were arguably better than were obtained with nerve grafts. A similar conclusion can be drawn from the result found using both rhGGF-2 and SC’s in PHB conduits 4 months after axotomy. In summary, these findings reinforce the significance of sensory neuronal death in peripheral nerve trauma, and the possibility of its` limitation by early nerve repair. Two agents for the adjuvant therapy of such injuries were identified, that can virtually eliminate neuronal death, and enhance regeneration. Elements in the creation of a bioartificial nerve conduit to replace, or surpass autologous nerve graft for secondary nerve repair are presented.

The developing nervous system depends largely on extracellular cues to shape its complex network of neurons. Classically, neurotrophins are known to be important mediators in this process. More recently, Bone Morphogenetic Proteins (BMPs), belonging to the Transforming Growth Factor beta (TGFβ) superfamily of secreted cytokines, have been shown to exert a wide range of effects, such as cellular growth, differentiation, survival and apoptosis, both in the developing and adult nervous system. They signal via serine/threonine kinase receptor essentially to the Smad pathway, which carries the signal to the nucleus where the transcription of target genes is regulated. This thesis investigates the functions of BMPs in the nervous system, using a set of different models. Firstly, a targeted deletion of GDF10 (BMP3b) in the mouse was established to evaluate the role of this growth/differentiation factor in the hippocampal formation, a brain area known to be involved in memory processing. Other members of the TGFβ superfamily likely compensate for the lack of GDF10, since no detectable alterations in hippocampal function or gene transcription profile have been found. Secondly, a mouse model was set up, with the aim to study impaired BMP-signalling in dopaminergic neurons. The tyrosine hydroxylase (TH) locus was used to drive the expression of dominant negative BMP receptors by means of bicistronic mRNAs. TH is the rate-limiting enzyme in the biosynthesis of catecholamine and the mice described, show a graded decrease of TH-activity resulting in severe to mild dopamine deficiency. The contribution of the dominant negative BMP receptors to the phenotype is however secondary to the apparent TH hypomorphism. The final theme of this thesis is the potentiating effects of BMPs on neurotrophin-induced neurite outgrowth as studied in explanted ganglia from chick embryos and in the rat phaeochromocytoma cell line PC12. A number of pharmacological inhibitors of intracellular signalling kinases were applied to the cultures in order to reveal the contribution of different pathways to the enhanced neurite outgrowth. We made the unexpected finding that inhibition of MEK signalling mimicked the potentiating effects of BMP stimulation in the chick system. The underlying mechanisms for the synergistic effects, however, are still an enigma.

Bakgrund: Smärtor i ben är vanligt förekommande och neuropati (nervskada) är en orsak som troligen är underdiagnostiserad. Bimanuell (tvåhändig/tvåsidig) nervpalpation och känseltest med sporre har visat sig vara ganska tillförlitliga och enkla test för att hitta nervskada men har inte testats på friska individer. Syfte: Syftet var att undersöka om bimanuell nervpalpation i fossa poplitea framkallar smärta/obehag och om det finns skillnad mellan vänster och höger sida vid bimanuell undersökning med sporre på underben hos friska försökspersoner. Metod: Ett bimanuellt palpationstest av nervi tibialis och peroneus i fossa poplitea och även ett bimanuellt känseltest med sporre över dermatomen L4, L5 och S1 på underben genomfördes. Urvalet var ändamålsenligt och totalt deltog 37 försökspersoner. Åldersspannet var 20 till 57 och medianålder 23. Resultat: Vid palpationstestet hade intensiteten av smärta/obehag en median på 1 (variationsvidd 3) på den 11 gradiga skalan. En stor del skattade olika mellan sidorna i både palpationstestet (11 av 37) och känseltestet med sporre (25 av 37). Det var inte någon större skillnad mellan könen. Slutsats: När man utför dessa nervtester måste man ta hänsyn till att även friska individer ofta anger en liten sidoskillnad och inte alltid skattar noll vad gäller smärta/obehag. Det behövs dock fler studier för att bekräfta dessa resultat. / Background: Leg pain is common and neuropathy (nerve disease) is one reason which probably is under diagnosed. Bimanual (bilateral) nerve palpation and sensory test with spurs has been shown to be quite reliable. Furthermore, the tests are straight forward detecting nerve disease but have not been tested on a healthy population. Purpose: The purpose was to investigate whether peripheral nerve palpation in fossa poplitea induces pain/discomfort, and if side difference exists in a sensibility test with spurs on the lower leg in healthy subjects. Method: A bimanual palpation test of the tibial and peroneal nerve in fossa poplitea and also a bimanual sensibility test with spurs of dermatome L4, L5 and S1 on the lower leg were carried out. In order to find healthy subjects a purposive sampling was made. A total of 37 subjects between 20 and 57 years with a median age of 23 participated in the study. Results: At the palpation test the intensity of pain/discomfort had a median of 1 (range 3) in the 11 degrees of pain scale. A large part estimated differences between the sides in both the palpation test (11 of 37) and the sensibility test with spur (25 of 37). There was no significant difference between the sexes. Conclusion: When performing these nerve tests it is important to keep in mind that even healthy individuals might perceive some pain/discomfort as well as side difference. However, we need more studies to confirm these results.

Syfte: Att identifiera behovet för arbetsterapi i Nehemiah Autism Center genom att utföra en behovsanalys. Metod: Mixad-metod användas för att utveckla en passande behovsanalys för att identifiera behovet för arbetsterapi. Resultat: Alla områden där en arbetsterapeut kan bidrag till valdes. Kommunikation och sociala färdigheter rapporterades mest frekvent och beteende förvaltning rankades som viktigast bland vårdnadshavare. Bland anställda, fritid och lek rapporterades mest frekvent och stresshantering rankades som viktigast. Utbildningsmöjligheter, kommunikation mellan anställda och medarbetare relation identifierades som stödjande faktorer för att uppnå målet på Nehemiah Autism Center. Stigma, religion och kulturell mångfald rapporterades som icke-stödjande faktorer för att uppnå målet på Nehemiah Autism Center. Slutsats: Det finns ett behov för arbetsterapi för att möta behovet hos barn med autism på Nehemiah Autism Center i Addis Ababa, Etiopien. / Aim: To identify the occupational therapy needs at the Nehemiah Autism Center by completing a needs assessment. Method: A mixed-methods design was adopted to construct a comprehensive needs assessment to identify the occupational therapy needs. Result: All areas of what an occupational therapist could assist with were selected as an area of need. Communication and social skills were most frequently reported and behavior management was ranked as most important among caregivers. Among staff members, leisure and play was reported most frequently and stress management was ranked as most important. Training opportunities, communication among staff members, and co-worker relationship were identified to be supporting factors in achieving the goal at Nehemiah Autism Center. Stigma, religion, and cultural diversity were reported to be unsupportive factors in achieving the goal at Nehemiah Autism Center. Conclusion: There is a great need for occupational therapy services to attend to children with autism spectrum disorder at Nehemiah Autism Center in Addis Ababa, Ethiopia.

Bakgrund: Efter Pandemrix-vaccinationen år 2009 i Sverige insjuknade ett stort antal unga individer i den koniska sjukdomen narkolepsi. Syfte: Kartlägga aktivitetsvanor, stillasittande, tilltro till egen förmåga att klara fysisk aktivitet samt undersöka samband mellan aktivitetsnivå och tilltro till egen förmåga att klara fysisk aktivitet. Metod: Undersökningsgruppen var 120 individer över 18 år, från Narkolepsiföreningen, som drabbats i samband med Pandemrix-vaccinationen år 2009. Datainsamling genomfördes via enkät.   Resultat: 47,1 procent uppnådde WHO:s rekommenderade aktivitetsnivå. 25,2 procent var fysiskt aktiva mindre än en gång i månaden eller aldrig. Genomsnittlig stillasittandetid var sju timmar och nio minuter/dag. Medianen för tilltro till egen förmåga att klara fysisk aktivitet var 19 på en skala mellan 9-36. Ett signifikant måttligt samband mellan tilltro till egen förmåga att klara fysisk aktivitet och aktivitetsnivå förelåg. Konklusion: Studiens resultat talar för att narkolepsidrabbade bör öka sin aktivitetsnivå och för att uppnå det även öka tilltro till egen förmåga att klara fysisk aktivitet. / Backgroud: After the Pandemrix-vaccination in 2009 a sudden increase in childhood narcolepsy was observed in Sweden. Scientific research focusing on the level of physical activity within this group is scarce. Purpose: Identifying the level of physical activity and physical exercise, sedentary behavior, self-efficacy to perform physical activity, as well as examine the correlation between physical activity level and self-efficacy to perform physical activity. Method: 120 individuals, over 18 years of age, who developed narcolepsy due to the Pandemrix-vaccination and were members of the Swedish Narcolepsy Association participated in the study. The data collection was conducted through a survey. Results: 47.1 percent of the participants achieved the WHO recommendations for physical activity. 25.2 percent were physically active less than once a month or never. The duration of the participants average time of sedentary behavior was seven hours and nine minutes per day. The median for self-efficacy to perform physical activity was 19 on a scale between 9-36. There was a significant moderate correlation between the participants self-efficacy to perform physical activity and their level of physical activity . Conclusion: The results of this study indicates that individuals suffering from narcolepsy should increase their level of physical activity as well as increase their self-efficacy to perform physical activity.

Alzheimer’s disease (AD) is a neurodegenerative disease and the major cause of dementia, affecting more than 50 million people worldwide. Chronic pain is long-lasting, persistent pain that affects more than 1.5 billion of the world population. Overlapping and heterogenous symptoms of AD and chronic pain conditions complicate their diagnosis, emphasizing the need for more specific biomarkers to improve the diagnosis and understand the disease mechanisms. To characterize disease pathology of AD, we measured the protein changes in the temporal neocortex region of the brain of AD subjects using mass spectrometry (MS). We found proteins involved in exo-endocytic and extracellular vesicle functions displaying altered levels in the AD brain, potentially resulting in neuronal dysfunction and cell death in AD. To detect novel biomarkers for AD, we used MS to analyze cerebrospinal fluid (CSF) of AD patients and found decreased levels of eight proteins compared to controls, potentially indicating abnormal activity of complement system in AD. By integrating new proteomics markers with absolute levels of Aβ42, total tau (t-tau) and p-tau in CSF, we improved the prediction accuracy from 83% to 92% of early diagnosis of AD. We found increased levels of chitinase-3-like protein 1 (CH3L1) and decreased levels of neurosecretory protein VGF (VGF) in AD compared to controls. By exploring the CSF proteome of neuropathic pain patients before and after successful spinal cord stimulation (SCS) treatment, we found altered levels of twelve proteins, involved in neuroprotection, synaptic plasticity, nociceptive signaling and immune regulation. To detect biomarkers for diagnosing a chronic pain state known as fibromyalgia (FM), we analyzed the CSF of FM patients using MS. We found altered levels of four proteins, representing novel biomarkers for diagnosing FM. These proteins are involved in inflammatory mechanisms, energy metabolism and neuropeptide signaling. Finally, to facilitate fast and robust large-scale omics data handling, we developed an e-infrastructure. We demonstrated that the e-infrastructure provides high scalability, flexibility and it can be applied in virtually any fields including proteomics. This thesis demonstrates that proteomics is a promising approach for gaining deeper insight into mechanisms of nervous system disorders and find biomarkers for diagnosis of such diseases.

Alzheimers sjukdom är den vanligaste orsaken till demens och i samband med att befolkningen blir större och allt äldre ökar även antalet patienter. Vid sjukdomen sker en hjärnatrofi och de mikroskopiska fynd man ser är extracellulära plack av β-amyloid, intracellulära neurofibriller av fosforylerat tau och förlust av nervcellsutskott, axoner, synapser och dendriter. Några av de tidiga patologiska förändringarna man kan se är störningar i nervcellernas lysosomala system som fyller en viktig roll vid nedbrytning av makromolekyler. I en tidigare studie har man påvisat förhöjda nivåer av proteiner från det lysosomala systemet i cerebrospinalvätska. Syftet med den här studien var att mäta nivåer av det lysosomala systemets proteiner i human hjärnvävnad från patienter med Alzheimer och jämföra dessa med kontrollprover. De sex proteiner som analyserades med Western blot var EEA1, PICALM, LAMP-1, LAMP-2, LC3 och TFEB. Resultaten visar på signifikant ökning i temporala cortex av LAMP-1 och LAMP-2 och en signifikant minskning av LC3 och EEA1 hos patienter med Alzheimers sjukdom. För att kunna dra riktiga slutsatser kring hur de ökade nivåerna i cerebrospinalvätska speglar de olika sjukdomsmekanismerna i hjärnan krävs vidare analyser av fler patientprover samt prover från andra områden i hjärnan. / Alzheimer's disease is the most common cause of dementia, and when the population becomes larger and older also the number of patients increase. A cerebral atrophy and microscopic findings of extracellular plaques of β-amyloid, intracellular neurofibrillary of phosphorylated tau and loss of nerve cell protrusions, axons, synapses and dendrites are seen during the disease. One of the early pathological changes is the disruption of the neuronal lysosomal network that plays an important role in the degradation of macromolecules. In a previous study elevated levels of proteins of the lysosomal network in cerebrospinal fluid from Alzheimer’s disease patients was demonstrated. The purpose of this study was to measure levels of the lysosomal network system in the brain. The six proteins EEA1, PICALM, LAMP-1, LAMP -2, LC3 and TFEB were analyzed in human brain tissue from five Alzheimer's disease cases and five control cases by Western blot. The results show a significant increase in the temporal cortex of LAMP-1 and LAMP -2 and a significant decrease of LC3 and EEA1 in patients with Alzheimer's disease. In order to draw proper conclusions about how the increased levels in cerebrospinal fluid reflect the different disease mechanisms in the brain it requires further analysis of more patient samples and from other areas of the brain.

Syfte: Syftet med denna studie var att undersöka sambandet mellan fysisk aktivitetsnivå, depressiva symtom och funktionshinder hos personer med Parkinsons sjukdom. Därtill kartlägga fysisk aktivitetsnivå, depressiva symtom samt funktionshinder bland personer med Parkinsons. Bakgrund: Parkinsons sjukdom är en av de mest förekommande neurodegenerativa sjukdomarna. Sjukdomen är kopplad till både motoriska och icke-motoriska symtom såsom depressiva symtom. Metod: 30 personer inkluderades i denna studie. I denna studie användes IPAQ-SF för att mäta fysisk aktivitetsnivå, MADRS-S för att mäta depressiva symtom samt WHODAS 2.0 för att skatta funktionshinder. Formulären sammanställdes i en webbenkät som publicerades via länk på Facebooksidor ägnade åt Parkinsons sjukdom. Resultat: Utav inkluderade i studien hade 4 (13.3%) låg fysisk aktivitetsnivå, 13 (43.3%) måttlig samt 13 (43.3%) hög. 16 (53.3%) klassades som väsentligen obesvärad, 11 (36.7%) som mild depression, 3 (10.0%) som måttlig samt ingen som svår depression. Bland de inkluderade var medianen för WHODAS 2.0 enligt följande: förstå och kommunicera 3.5 (2.0-5.0), förflyttning 4.5 (2.5-6.5), personlig vård 2.0 (2.0-3.5), relationer 4.0 (3.0-5.5), dagliga aktiviteter 4.5 (3.0-6.5) samt delaktighet i samhället 4.0 (3.0-6.0). Sambandet mellan fysisk aktivitetsnivå och depressiva symtom gav r=0.31 p=0.10. Sambandet mellan fysisk aktivitetsnivå och funktionshinder visade r=0.45 p=0.02. Sambandet mellan depressiva symtom och funktionshinder visade r=0.74 p=0.01. Slutsatser: En måttlig till hög fysisk aktivitetsnivå var vanligt. Likaså var förekomsten av depression omfattande. Förekomsten av funktionshinder var därutöver relativt låg. Korrelationen mellan samtliga variabler anses vara låg frånsett den mellan depressiva symtom och funktionshinder, vilken var måttlig. / Aim: The aim of this study is to explore the correlation between physical activity level, depressive symptoms and health and function in persons with Parkinson’s disease. In addition, this study aims to examine and map physical activity level, depressive symptoms and health and function among persons with Parkinson’s disease. Background: Parkinson’s disease is one the most widespread neurodegenerative diseases. The disease can present itself in either motor or non-motor symptoms, such as depressive symptoms. Method: 30 participants were included in this study. IPAQ-SF was used to measure physical activity level, MADRS-S to measure depressive symptoms and WHODAS 2.0 to measure health and function. The questionnaires were compiled in a web survey which was then posted on various Facebook pages aimed at Parkinson’s disease. Results: Among participants included 4 (13.3%) had low physical activity level, 13 (43.3%) moderate and 13 (43.3%) high. 16 (53.3%) were classed as having no depression, 11 (36.7%) as mild depression, 3 (10.0%) as moderate and none as severe depression. The median for the respective domain of were as follows: cognition 3.5 (2.0-5.0), mobility 4.5 (2.5-6.5), self care 2.0 (2.0-3.5), getting along with people 4.0 (3.0-5.5), life activities 4.5 (3.0-6.5), participation 4.0 (3.0-6.0). The correlation between physical activity level and depressive symptoms provided r=0.31 p=0.10, physical activity level and health and function r=0.45 p= 0.02 and depressive symptoms and health and function r=0.74 p=0.01. Conclusions: This study demonstrated a prominent occurance of high and moderate levels of physical activity. Likewise, the prevalence of depression was extensive. In addition, the incidence of disability was apparently low. The correlation between all variables is considered to be low apart from that between depressive symptoms and disability, which was moderate.