Experience of establishing an acute geriatric outreach service versus subacute service to nursing homes.

To share our experience of establishing an acute outreach service to nursing homes and to evaluate the impact of such service on emergency department presentations, data were drawn from a pre-existing database from 2013 to 2017. Of the 986 acute patients treated in 12 nursing homes over a 23-month period, the acute geriatric outreach service was shown to be safe, with few adverse events (one allergic reaction) and 5.3% of patients required transfer to hospital. The acute service decreased emergency department presentation of nursing home patients by 10% compared to the subacute service (incidence rate ratio = 0.90; 95% confidence interval: 0.84-0.96; P = 0.001). Cost-benefit analysis showed for every $1 spent, a saving of $5 was realised.

Genetic and environmental factors in vascular dementia: an update of blood brain barrier dysfunction.

Vascular dementia (VaD) describes a combination of both cognitive and behavioural manifestations associated with variable brain lesions of vascular origin. While vascular risk factors have been implicated in VaD, the relationship is most evident when the factors are considered together and not individually. This review will examine the significance of the integrity of blood brain barrier (BBB) tight junction (TJ) proteins - occludin and claudins in the pathophysiology of VaD. Specifically, some of the genetic contributors to VaD, namely those responsible for the integrity of the BBB, will be reviewed in detail. Moreover, environmental factors will be considered in conjunction with these genes to examine how the interaction of environmental and genetic factors contributes to one's susceptibility to VaD.

Falls prevention in the elderly: translating evidence into practice.

Falls are a common problem in the elderly. A common error in their management is that injury from the fall is treated, without finding its cause. Thus a proactive approach is important to screen for the likelihood of fall in the elderly. Fall assessment usually includes a focused history and a targeted examination. Timed up-and-go test can be performed quickly and is able to predict the likelihood of fall. Evidence-based fall prevention interventions include multi-component group or home-based exercises, participation in Tai Chi, environmental modifications, medication review, management of foot and footwear problems, vitamin D supplementation, and management of cardiovascular problems. If possible, these are best implemented in the form of multifactorial intervention. Bone health enhancement for residential care home residents and appropriate community patients, and prescription of hip protectors for residential care home residents are also recommended. Multifactorial intervention may also be useful in a hospital and residential care home setting. Use of physical restraints is not recommended for fall prevention.

Preventing aspiration pneumonia in older people: do we have the 'know-how'?

Aspiration pneumonia is common in older people. To reduce the risk of aspiration pneumonia, maintenance of good oral hygiene is important and medications affecting salivary flow or causing sedation are best avoided, if possible. The use of H2 blockers and proton-pump inhibitors should be minimised. Different compensatory and facilitation techniques can be applied during oral feeding. Hand feeding should be tried before consideration of tube feeding. The use of tube feeding is the last resort and is mainly for improving nutrition and hydration. Prevention of aspiration pneumonia and increasing survival rates should not be the rationales for tube feeding. Feeding via both gastrostomy and nasogastric tube has similar risks for aspiration pneumonia, and continuous pump feeding is not better than intermittent feeding. Jejunal feeding might decrease the chance of aspiration pneumonia in selected high-risk patients. If older patients are on angiotensin-converting enzyme inhibitors without intolerable cough, continuing the drug may be beneficial. Folate deficiency, if present, needs to be promptly corrected. Further better-designed studies are warranted to find the best ways for prevention of aspiration pneumonia.

Preferences, barriers and facilitators for establishing comprehensive stroke units: a multidisciplinary survey.

OBJECTIVES: To determine the preferences of multidisciplinary stroke clinicians for models of inpatient stroke unit care and perceived barriers to establishing a comprehensive stroke unit (CSU) model (acute and rehabilitation care in the same ward). METHODS: Written questionnaires distributed and completed at multidisciplinary stroke unit case conferences in NSW, Australia. RESULTS: Twenty hospitals with 22 stroke units were surveyed, 13 acute stroke units, 7 rehabilitation stroke units, 2 CSUs. Two hundred and twenty-eight respondents: 99 (43.4%) allied health, 72 (31.6%) nurses and 57 (25.0%) doctors. One hundred and fifty-one respondents (67.0%) thought CSU to be the best model. Seventy-three % of doctors and 79% of allied health preferred CSU v. 57% of nurses (P=0.041). Of doctors, rehabilitation specialists were most likely to favour comprehensive model (84.2%) and neurologists least (57.0%). The main perceived advantages of CSU were reduced cost and improved functional outcomes; perceived disadvantages were increased workload and unwell patients unable to participate in rehabilitation. Main perceived barriers to establishing CSU were lack of space, money, staffing and time. CONCLUSION: Although most current stroke unit care in NSW is based on the traditional model of acute and rehabilitation components in separate wards or hospitals, the majority of multidisciplinary stroke team clinicians believe CSU is the optimum model. What is known about the topic? Stroke unit care is known to improve survival and dependency but the optimum model of care is unproven, despite some small studies suggesting that the CSU model may result in better outcomes. What does this paper add? This paper is the first to survey stroke clinicians from various disciplines and types of unit, to determine their preferences for stroke unit model. What are the implications for practitioners? A majority of clinicians expressed a preference for the CSU model, suggesting that most would be comfortable caring for patients in both acute and rehabilitation phases of stroke care if further such units are established.

Study protocol for a phase III randomised controlled trial of Sailuotong (SLT) for vascular dementia and Alzheimer's disease with cerebrovascular disease.

Vascular dementia (VaD) accounts for 15-20% of all dementia cases. It is a syndrome of acquired cognitive impairment with a complex pathophysiological basis. A novel herbal formulation (Sailuotong; SLT) consisting of Panax ginseng C.A Mey, Ginkgo biloba L and Crocus sativus L extracts was developed to treat VaD. Preclinical animal studies found significant improvements in memory and in pathogenic biochemical parameters. Appropriate safety of SLT was shown in acute and chronic toxicity studies, and early clinical trials of SLT demonstrated enhancements in cognition in VaD patients. A fully powered study with a long intervention period is needed to confirm the efficacy and safety of this novel intervention. A rigorous phase III clinical trial was developed with the aim of recruiting 238 patients diagnosed with mild to moderate probable VaD, or VaD mixed with Alzheimer's disease (where cerebrovascular disease is the clinical dominant contributor to dementia, abbreviated as CVD+AD). Using a permuted block strategy, participants will be randomly allocated to receive SLT (120 mg bd) or placebo capsules for an intervention period of 52 weeks and will be followed-up for an additional 13 weeks. The primary outcome measures are the Vascular Dementia Assessment Scale-cognitive subscale and Alzheimer's Disease Cooperative Study-Activities of Daily Living scale. Secondary outcome measures include the Clinician's Interview Based Impression of Change-Plus, CLOX, EXIT-25, Neuropsychiatric Inventory-Clinician rating scale, and Dementia Quality of Life questionnaire. Safety is assessed through adverse event reports and liver, renal, and coagulation studies. Primary and secondary outcome measures will be compared between treatment and placebo groups, using intention to treat and per protocol analyses. We hypothesise that a 52-week treatment of SLT will be clinically effective and well tolerated in participants with VaD or AD+CVD. This project will provide vital efficacy and safety data for this novel treatment approach to VaD.

Telemedicine vs Face-to-Face for Nursing Home Residents With Acute Presentations: A Noninferiority Study.

OBJECTIVES: Telemedicine and face-to-face outreach services to nursing homes (NHs) have been used to reduce hospital utilization rates for acute presentations. However, how these modalities compare against each other is unclear. This article examines if the management of acute presentations in NHs with care involving telemedicine is noninferior to care delivered face-to-face. DESIGN: A noninferiority study was conducted on a prospective cohort. Face-to-face intervention involved on-site assessment by a geriatrician and aged care clinical nurse specialist (CNS). Telemedicine intervention involved on-site assessment by an aged care CNS with telemedicine input by a geriatrician. SETTING AND PARTICIPANTS: A total of 438 NH residents with acute presentations from 17 NHs between November 2021 and June 2022. METHODS: Between-group differences in proportion of residents successfully managed on-site and mean number of encounters were evaluated using bootstrapped multiple linear regression; 95% CIs were compared against predefined noninferiority margins with noninferiority P values calculated. RESULTS: In the adjusted models, care involving telemedicine demonstrated noninferiority in the difference in proportion of residents successfully managed on-site (95% CI lower limit -6.2% to -1.4% vs -10% noninferiority margin; P < .001 for noninferiority) but not in the difference in mean number of encounters (95% CI upper limit 1.42 to 1.50 encounters vs 1 encounter noninferiority margin; P = .7 for noninferiority). CONCLUSIONS AND IMPLICATIONS: In our model of care, care that involved telemedicine was noninferior to care delivered face-to-face in managing NH residents with acute presentations on-site. However, additional encounters may be required. Application of telemedicine ought to be tailored to fit the needs and preferences of stakeholders.

Involvement of single nucleotide polymorphisms of junction adhesion molecule with small vessel vascular dementia.

Objectives: It is now recognized that blood brain barrier (BBB) leakage occurs in cerebral small vascular disease (CSVD) and plays a significant role in the pathophysiology of vascular dementia. We hypothesized that genetic polymorphisms of junctional adhesion molecule-A (JAM-A) (which may result in compromised structure of tight junction proteins that form the BBB) in combination with cerebrovascular risk factors hypertension, lipid disorders, and type 2 diabetes may result in BBB leakage and increase the individual's risk of CSVD-related dementia. Methods: In this case-control study, 97 controls with a mean Mini-Mental State Exam (MMSE) score of 29 and 38 CSVD-related vascular dementia participants (mean MMSE score of 19) were recruited. Bloods were collected for the analysis of two common single nucleotide polymorphisms (SNPs) of the JAM-A genotypes rs790056 and rs2481084 using real-time polymerase chain reaction (PCR) assay. Medical history of hypertension, hyperlipidemia, and diabetes was collected for all participants. Results: Polymorphisms of genotype JAM-A SNP rs790056 showed statistically significant result when the subgroup with hyperlipidemia was analyzed (OR = 3.130, p = 0.042 for TC + CC genotypes with hyperlipidaemia vs controls). Similar result was found with diabetes (OR = 4.670, p = 0.031 for TC + CC genotypes vs controls). No significant result was found with hypertension. Borderline results of statistical significance were found for JAM-A SNP rs2481084 with hyperlipidemia (OR = 3.210, p = 0.054 for TC + CC genotypes vs controls) and with diabetes (OR = 3.620, p = 0.069 for TC + CC genotypes vs controls) but not for hypertension. The borderline results might have been due to lack of statistical power because of small sample size. Conclusions: These results lend further support that cerebrovascular risk factors interact with genetic polymorphisms of BBB proteins to increase the risk of vascular dementia.

Frontotemporal dementia - features, diagnosis and management.

BACKGROUND: Frontotemporal dementia is the third or fourth most common form of dementia in the 45-65 years age group. It causes significant morbidity as well as a six to eightfold increase in mortality risk. OBJECTIVE: This article provides an overview of the pathophysiology of frontal lobe function and the genetics of frontotemporal dementia. It also summarises the clinical features, diagnosis and management of frontotemporal dementia. DISCUSSION: While the clinical presentation of frontotemporal dementia was described as early as the nineteenth century, recent advances in genetics have resulted in greater understanding of the pathophysiology of this disease. While imaging may support the diagnosis of frontotemporal dementia, it is essentially a clinical diagnosis based on the presence of typical clinical features and the findings of neuropsychological tests. Clinical management of frontotemporal dementia remains a challenge and is largely centred on behavioural management. Pharmacological agents such as selective serotonin reuptake inhibitors and antipsychotics may be helpful, although evidence to support their use is minimal.

Plasma lipidomic biomarker analysis reveals distinct lipid changes in vascular dementia.

Vascular dementia (VaD) is a complex neurocognitive disorder secondary to a variety of cerebrovascular lesions. Numerous studies have shown that lipid metabolism is involved in the pathobiology of the disease. We examined the plasma lipid profiles in VaD, with the expectation of identifying reliable lipid biomarkers for VaD. 49 VaD patients and 48 healthy controls were recruited from Bankstown-Lidcombe Hospital in Sydney, Australia. Lipids were extracted by single phase 1-butanol/methanol, and untargeted analysis was performed by liquid chromatography coupled-mass spectrometry (LC-MS/MS). Univariate analysis of variance was used to examine the differences in lipid classes and individual lipids between VaD and control groups. In an independent sample of 161 subjects from the Older Australian Twins Study (OATS), elastic net penalization for the generalized linear model (Glmnet) and Random Forest were applied to the lipid levels to subcategorise the sample into vascular cognitive impairment and controls. Most lipids belonging to the classes of ceramides (Cer), cholesterol esters (ChE) and phospholipids were significantly lower in VaD plasma, while glycerides were elevated compared to controls. Levels of ChE, Cer and the two lipid classes together achieved the best accuracy in discriminating VaD from controls, with more than 80% accuracy. The probable VaD group in the OATS sample predicted by the lipid levels showed greater impairment in most cognitive domains, especially attention and processing speed and executive function from controls but did not differ in white matter hyperintensities and DTI measures. As a conclusion, plasma lipids levels, in particular Cer and ChE, are abnormal in VaD and may help discriminate them from healthy controls. Understanding the basis of these differences may provide insights into the pathobiology of VaD.

The Precursor to Glutathione (GSH), γ-Glutamylcysteine (GGC), Can Ameliorate Oxidative Damage and Neuroinflammation Induced by Aß40 Oligomers in Human Astrocytes.

Glutathione (GSH) is one of the most abundant thiol antioxidants in cells. Many chronic and age-related diseases are associated with a decline in cellular GSH levels or impairment in the catalytic activity of the GSH biosynthetic enzyme glutamate cysteine ligase (GCL). γ-glutamylcysteine (GGC), a precursor to glutathione (GSH), can replenish depleted GSH levels under oxidative stress conditions, by circumventing the regulation of GSH biosynthesis and providing the limiting substrate. Soluble amyloid-ß (Aß) oligomers have been shown to induce oxidative stress, synaptic dysfunction and memory deficits which have been reported in Alzheimer's disease (AD). Calcium ions, which are increased with age and in AD, have been previously reported to enhance the formation of Aß40 oligomers, which have been casually associated with the pathogenesis of the underlying neurodegenerative condition. In this study, we examined the potential beneficial effects of GGC against exogenous Aß40 oligomers on biomarkers of apoptosis and cell death, oxidative stress, and neuroinflammation, in human astrocytes. Treatment with Aß40 oligomers significantly reduced the cell viability and apoptosis of astrocyte brain cultures and increased oxidative modifications of DNA, lipids, and protein, enhanced pro-inflammatory cytokine release and increased the activity of the proteolytic matrix metalloproteinase enzyme, matric metalloproteinase (MMP)-2 and reduced the activity of MMP-9 after 24 h. Co-treatment of Aß40 oligomers with GGC at 200 µM increased the activity of the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx) and led to significant increases in the levels of the total antioxidant capacity (TAC) and GSH and reduced the GSSG/GSH ratio. GGC also upregulated the level of the anti-inflammatory cytokine IL-10 and reduced the levels of the pro-inflammatory cytokines (TNF-α, IL-6, and IL-1ß) and attenuated the changes in metalloproteinase activity in oligomeric Aß40-treated astrocytes. Our data provides renewed insight on the beneficial effects of increased GSH levels by GGC in human astrocytes, and identifies yet another potential therapeutic strategy to attenuate the cytotoxic effects of Aß oligomers in AD.

Aged care services in Australia and commentary on lessons learnt.

The Australian aged care service is a mature and evolving service. It is comprehensive with good continuity of care between hospital and community. Innovative models of care that are built on the principles of improved efficiency, better quality, and safety are constantly being introduced as our population is aging, resulting in higher demand in our healthcare services and increasing healthcare cost. Collaborative effort of a multidisciplinary team underpins our successful aged care model as most of our older patients have multiple comorbidities with various functional and psychosocial needs. General practitioners play an important role in the care of older patients in the community.

Cerebral small vessel disease and the risk of Alzheimer's disease: A systematic review.

BACKGROUND: Cerebral small vessel disease (CSVD) comprises a variety of disorders affecting small arteries and microvessels of the brain, manifesting as white matter hyperintensities (WMHs), cerebral microbleeds (CMBs), and deep brain infarcts. In addition to its contribution to vascular dementia (VaD), it has also been suggested to contribute to the pathogenesis of Alzheimer's disease (AD). METHOD: A systematic review of the literature available on Medline, Embase and Pubmed was undertaken, whereby CSVD was divided into WMHs, CMBs and deep brain infarcts. Biomarkers of AD pathology in the cerebrospinal fluid or plasma, or positron emission tomographic imaging for amyloid and/or tau deposition were used for AD pathology. RESULTS: A total of 4117 articles were identified and 41 articles met criteria for inclusion. These consisted of 17 articles on vascular risk factors for clinical AD, 21 articles on Aß pathology and 15 articles on tau pathology, permitting ten meta-analyses. CMBs or lobar CMBs were associated with pooled relative risk (RR) of AD at 1.546, (95%CI 0.842-2.838, z = 1.41 p = 0.160) and 1.526(95%CI 0.760-3.063, z = 1.19, p = 0.235) respectively, both non-significant. Microinfarcts were associated with significantly increased AD risk, with pooled odds ratio OR at 1.203(95%CI 1.014-1.428, 2.12 p = 0.034). Aß pathology was significantly associated with WMHs in AD patients but not in normal age-matched controls. The pooled ß (linear regression) for total WMHs with CSF Aß42 in AD patients was -0.19(95%CI -0.26-0.11, z = 4.83 p = 0.000) and the pooled r (correlation coefficient) for WMHs and PiB in the normal population was -0.10 (95%CI -0.11-0.30, 0.93 p = 0.351). CMBs were significantly associated with Aß pathology in AD patients. The pooled standardized mean difference (SMD) was -0.453, 95%CI -0.697- -0.208, z = 3.63 p = 0.000. There was no significant relationship between the incidence of lacunes and levels of CSFAß, with a pooled ß of 0.057 (95%CI -0.050-0.163, z = 1.05 p = 0.295). No significant relationship was found between CMBs and the levels of CSFt-tau/CSFp-tau in AD patients (-0.014, 95%CI -0.556-0.529, z = 0.05 p = 0.960; -0.058, 95%CI -0.630-0.515, z = 0.20 p = 0.844) and cortical CMBs and CSF p-tau in the normal population (0.000, 95%CI -0.706-0.706, z = 0.00 p = 0.999). CONCLUSIONS: Some CSVD markers were significantly associated with clinical AD pathology and may be associated with Aß/tau pathology. WMHs and microinfarcts were associated with increased risk of AD. It remains unclear whether they precede or follow AD pathology.

A functional polymorphism in the parkin gene promoter affects the age of onset of Parkinson's disease.

Mutations in the parkin gene are the major cause of autosomal recessive early-onset forms of Parkinson's disease (PD). As reduced parkin expression might also affect the clinical course of idiopathic PD we investigated the effect of a low expressing allele in the parkin promoter region on the age at disease onset (AAO). Patients with PD (n=175) fulfilling standard diagnostic criteria were recruited by experienced neurologists at two movement disorders clinics in Sydney and Brisbane, Australia. DNA was extracted from whole blood and the -258 T/G polymorphism genotyped using PCR/RFLP. AAO effects were analysed using univariate ANOVA, binomial logistic regression modelling and Kaplan-Meier survival analysis. Subjects with the GG genotype (n=10, mean AAO=46.2+/-11.5 (S.D.) years) had a significantly lower mean AAO compared to the common TT genotype (n=104, mean AAO=56.1+/-12.7, p=0.02). There was no difference in mean AAO between the TT and TG individuals (n=61, mean AAO=55.3+/-11.6). Stratifying the sample by median AAO (55 years) revealed that the GG genotype was over-represented in the early-onset group (n=9, OR=18.6, 95% CI=1.41-245.3, p=0.03). We speculate that reduced expression of normal parkin protein may result in an early manifestation of PD symptoms.

Safety and low molecular weight heparin in older people in a hospital with ambulatory care.

UNLABELLED: To examine major bleeding and mortality rates of low molecular weight heparin (LMWH) and unfractionated heparin (UFH) for patients with pulmonary embolism (PE) and/or deep vein thrombosis (DVT), a retrospective review of the medical records for 286 patients who presented at a local hospital with PE and/or DVT during the period November 2002-August 2003 was performed. DATA COLLECTED: presence of co-morbidities, concurrent medications, presence, site and severity of bleeding, outcome. Of all the patients, 50.7% received LMWH plus warfarin, 21.0% received UFH plus LMWH plus warfarin, 14.0% received UFH and warfarin, and 9.8% received LMWH only. There were nine minor bleeds and six major bleeds, which resulted in four deaths. Being a hospitalized patient and being age > or =70 years were associated with a major bleed (p<0.05). For hospital inpatients age > or =70 years on UFH and LMWH the number of major bleeds/1000 patient days was 18.9 and 9.2, respectively. The major bleeding rate is comparable if not better than that reported in the literature in our hospital setting where nearly half of the anticoagulation services were provided as ambulatory care. The increased rate of bleeding in the elderly we found is consistent with the findings of previous studies.

Interference of α-Synuclein Uptake by Monomeric ß-Amyloid1-40 and Potential Core Acting Site of the Interference.

Increasing evidence suggests an important role of alpha-synuclein (α-Syn) in the pathogenesis of Parkinson's disease (PD). The inter-neuronal spread of α-Syn via exocytosis and endocytosis has been proposed as an explanation for the neuropathological findings of PD in sub-clinical and clinical phases. Therefore, interfering the uptake of α-Syn by neurons may be an important step in slowing or modifying the propagation of the disease. The purposes of our study were to investigate if the uptake of α-Syn fibrils can be specifically interfered with monomeric ß-Amyloid1-40 (Aß40) and to characterise the core acting site of interference. Using a radioisotope-labelled uptake assay, we found an 80 % uptake reduction of α-Syn fibrils in neurons interfered with monomeric Aß40, but not ß-Amyloid1-42 (Aß42) as compared to controls. This finding was further confirmed by enzyme-linked immunosorbent assay (ELISA) with α-Syn uptake reduced from about 80 % (Aß42) to about 20 % (Aß40) relative to controls. To define the region of Aß40 peptide capable of the interference, we explored shorter peptides with less amino acid residues from both the C-terminus and N-terminus. We found that the interference effect was preserved if amino acid residue was trimmed to position 11 (from N-terminus) and 36 (from C-terminus), but dropped off significantly if residues were trimmed beyond these positions. We therefore deduced that the "core acting site" lies between amino acid residue positions 12-36. These findings suggest α-Syn uptake can be interfered with monomeric Aß40 and that the core acting site of interference might lie between amino acid residue positions 12-36.

The origins of repetitive thought in rumination: separating cognitive style from deficits in inhibitory control over memory.

BACKGROUND AND OBJECTIVES: Rumination is a major contributor to the maintenance of affective disorders and has been linked to memory control deficits. However, ruminators often report intentionally engaging in repetitive thought due to its perceived benefits. Deliberate re-processing may lead to the appearance of a memory control deficit that is better explained as a difference in cognitive style. METHODS: Ninety-six undergraduate students volunteered to take part in a direct-suppression variant of the Think/No-Think paradigm after which they completed self-report measures of rumination and the degree to which they deliberately re-processed the to-be-suppressed items. RESULTS: We demonstrate a relation between rumination and impaired suppression-induced forgetting. This relation is robust even when controlling for deliberate re-processing of the to-be-suppressed items, a behavior itself related to both rumination and suppression. Therefore, whereas conscious fixation on to-be-suppressed items reduced memory suppression, it did not fully account for the relation between rumination and memory suppression. LIMITATIONS: The current experiment employed a retrospective measure of deliberate re-processing in the context of an unscreened university sample; future research might therefore generalize our findings using an online measure of deliberate re-processing or within a clinical population. CONCLUSIONS: We provide evidence that deliberate re-processing accounts for some--but not all--of the relation between rumination and suppression-induced forgetting. The present findings, observed in a paradigm known to engage top-down inhibitory modulation of mnemonic processing, provide the most theoretically focused evidence to date for the existence of a memory control deficit in rumination.

Identifying the pattern of olfactory deficits in Parkinson disease using the brief smell identification test.

BACKGROUND: Selective olfactory deficits occur in 70% to 90% of patients with Parkinson disease, independent of disease severity and duration. Olfactory testing may be a useful diagnostic aid for Parkinson disease, but the types of odors most commonly affected need to be identified. OBJECTIVE: To determine the pattern and types of odors affected in Parkinson disease by means of the University of Pennsylvania 12-item Brief Smell Identification Test (B-SIT; Sensonics, Inc, Haddon Heights, NJ). DESIGN: Testing patients with Parkinson disease and control subjects in 5 movement disorder clinics. PARTICIPANTS: Forty-nine nondemented patients with Parkinson disease and 52 age- and sex-matched controls. MAIN OUTCOME MEASURES: Normal or abnormal olfactory function was determined in each subject according to predetermined age and sex norms. Predictive statistics and discriminant function analyses were performed to determine the pattern and types of odors best discriminating patients from controls. RESULTS: Abnormal olfactory function was present in 40 (82%) of patients compared with 12 (23%) of controls. The B-SIT score was unaffected by smoking behavior, disease duration, or severity. The sensitivity of the B-SIT for Parkinson disease was 0.82, with a specificity and predictive value of 0.82 and 0.77, respectively. Only 5 of the 12 B-SIT odors (gasoline, banana, pineapple, smoke, and cinnamon) were required to adequately discriminate patients with Parkinson disease from controls. CONCLUSIONS: With the use of the B-SIT, 5 specific odors appear primarily affected in patients with Parkinson disease. Significantly, the ability of patients to detect some odors was unimpaired compared with that of controls. Better diagnostic aids could be developed on the basis of the selective pattern of hyposmia observed in Parkinson disease.

Genetics and Parkinson's disease.

Idiopathic Parkinson's disease is a neurodegenerative disorder that affects 1-2% of the population over the age of 65 years. Its aetiology is most likely a combination of complex genetic and environmental factors. Although Mendelian inheritance is seen in less than 5% of cases, recent studies have identified three genes mutations causing Parkinson's disease with a Mendelian inheritance pattern: autosomal dominantly inherited mutations of the alpha-synuclein gene on chromosome 4q21-q23, autosomal recessively inherited mutations of the parkin gene on chromosome 6q25.2-q27 and an autosomal dominantly inherited mutation of the Ubiquitin C-terminal hydrolase L1 (UCH-L1) gene on chromosome 4p14-15.1. A number of other candidate gene polymorphisms including cytochrome P450 2D6, N-acetyltransferase 2, monoamine oxidase-B and glutathione-s-transferase M1 are implicated in sporadic and familial cases and may also play a minor role in the aetiology of Parkinson's disease.