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ObjectiveWe aimed to examine whether impaired olfaction is associated with cognitive decline and indicators of neurodegeneration in the brain of dementia-free older adults.MethodsWithin the Rush Memory and Aging Project, 380 dementia-free participants (mean age = 78 years) were followed for up to 15 years, and underwent MRI scans. Olfactory function was assessed using the Brief Smell Identification Test (B-SIT) at baseline, and categorized as anosmia (B-SIT <6), hyposmia (B-SIT 6–10 in men and 6–10.25 in women), and normal (B-SIT 10.25–12 in men and 10.5–12 in women). Cognitive function was annually assessed with a battery of 21 tests, from which composite scores were derived. Structural total and regional brain volumes were estimated. Data were analyzed using linear regression and mixed-effects models.ResultsAt study entry, 138 (36.3%) had normal olfactory function, 213 (56.1%) had hyposmia, and 29 (7.6%) had anosmia. In multiadjusted mixed-effects models, hyposmia (β = −0.03, 95% confidence interval [CI] −0.05 to −0.02) and anosmia (β = −0.13, 95% CI −0.16 to −0.09) were associated with faster rate of cognitive decline compared to normal olfaction. On MRI, impaired olfaction (hyposmia or anosmia) was related to smaller volumes of the hippocampus (β = −0.19, 95% CI −0.33 to −0.05), and in the entorhinal (β = −0.16, 95% CI −0.24 to −0.08), fusiform (β = −0.45, 95% CI −0.78 to −0.14), and middle temporal (β = −0.38, 95% CI −0.72 to −0.01) cortices.ConclusionImpaired olfaction predicts faster cognitive decline and might indicate neurodegeneration in the brain among dementia-free older adults.

While recent studies suggest an important role of higher order olfactory brain areas for basic olfactory performance, the extent to which cortical and peripheral neural markers account for separate portions of the variability in olfactory perceptual acuity is still unclear. We addressed this question by correlating voxel-based morphometry data from 90 healthy adults with olfactory performance measures. Supplementing this approach with region of interest (ROI) analyses of functionally defined olfactory cortical regions and olfactory bulb volume, we sought to disentangle the relative contribution of central and peripheral areas to behavioral variability. Whole-brain analyses revealed a significant positive correlation of gray matter volume and olfactory function scores in the right orbital sulcus. This effect was confirmed by the ROI analyses, which further indicated a significant association of the olfactory score with olfactory bulb volume. Moreover, a functional dissociation was observed, with central and peripheral mechanisms explaining different aspects of the observed behavioral variance in the olfactory subscores. In line with previous clinical studies, these data thus suggest an important role of regional gray matter volume in the right orbitofrontal cortex and olfactory bulb volume for olfactory performance in healthy individuals.

Background:Olfactory dysfunction (OD) in old age is associated with poor health outcomes. Interrelationships among different correlates of OD can offer insights into the underlying mechanisms, but to date remain understudied.Methods:Odor identification performance and self-reported olfactory functioning were studied in 2,234 people aged 60–90 years, who were free of neurodegenerative disease and enrolled in the Swedish National Study on Aging and Care in Kungsholmen (SNAC-K) study, Stockholm, Sweden. OD was defined as the inability to identify more than 10 out of 16 odors (free or cued identification) in a standardized odor identification task. OD prevalence was estimated, and associations with demographic, genetic, vascular, clinical, and behavioral factors, as well as their interactions were examined using multiple logistic regression analyses.Results:Overall prevalence of OD was 24.8% (CI: 23.1; 26.6). Self-reports were characterized by low sensitivity (35%), but high specificity (87%). Advancing age (OR = 15.50, CI = 9.40; 26.10 between the first and last age group), and history of coronary heart disease (OR = 1.35, 95% CI = 1.04; 1.75) were the principal factors associated with an increased probability of OD, whereas female gender (OR = 0.53, 95% CI = 0.43; 0.66) and more years of education (OR = 0.97, CI 0.94; 0.99) were linked to a lower probability. Exploratory interaction analyses indicated that prevalence of OD was particularly elevated among Apolipropotein E (APOE) ε4 allele carriers who were also obese, and that being physically active counteracted the negative impact of cerebrovascular disease on OD.Conclusion:Demographic and genetic factors, but also prior and current health insults, are linked to OD in old age. Modulatory effects of behavioral factors highlight their value as possible prevention targets.

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Loss of olfactory function is common in old age, but evidence regarding qualitative olfactory dysfunction in the general older population is scarce. The current study investigates the prevalence and correlates of phantom smell experiences (phantosmia) in a population-based study (Swedish National Study on Aging and Care in Kungsholmen [SNAC-K]) of Swedish adults (n = 2569) aged between 60 and 90 years. Phantosmia was assessed through a standardized interview and defined as reporting having experienced an odor percept in the absence of any stimuli in the surrounding environment that could emit the odor. The relationships between phantosmia and demographic, genetic, health-related, and behavioral variables were analyzed with hierarchical logistic regression analyses. The overall prevalence of phantom smells was 4.9%, and was associated with female gender, carrying the met allele of the BDNF gene, higher vascular risk burden, and reporting distorted smell sensations (parosmia). Olfactory dysfunction was, however, not related to phantosmia. The most frequently reported phantom smell was smoky/burnt. A novel finding was that some individuals reported phantom smells with an autobiographical connotation. The results from this study indicate that the prevalence of phantosmia in the general older population is not negligible and that some factors that are beneficial for preserved olfactory function, such as female gender and the BDNF met allele, are also associated with the occurrence of phantom smells.

Clinical observations suggest that the experience of time phenomenology is disturbed in schizophrenia, possibly originating disorders in dynamic cognitive functions such as language or motor planning. We examined the subjective evaluation of temporal structure using an experimental approach involving judgments of simultaneity of simple, visually presented stimuli. We included a priming procedure, ie, a subthreshold presentation of simultaneous or asynchronous stimuli. This allowed us to evaluate the effects of subthreshold synchrony and to check for bias effects, ie, changes in the criteria used by the subjects to rate the stimuli. Primes were adapted to the responses of the subjects. Bias effects were thus expected to yield a change in the efficiency of the prime and to induce a change in the amplitude of the priming effect. Nineteen outpatients with schizophrenia and their individually matched controls participated in the study. In all tests, patients required longer delays between stimuli to detect that they were asynchronous. In other words, they judged stimuli to be synchronous even when their onset was separated by delays of 100 milliseconds and even more in some cases. These results contrasted with preserved effects of subthreshold synchrony. Our findings argue against the hypothesis that the patients' responses were influenced by biases. We conclude that the subjective evaluation of simultaneity/asynchrony is impaired in schizophrenia, thus leading to impairment in the phenomenology of event-structure coding. The method used in the present study provides a novel approach to the assessment of those disturbances related to time in patients with schizophrenia.

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