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Abnormal tau, a hallmark Alzheimer’s disease (AD) pathology, may appear in the locus coeruleus (LC) decades before AD symptom onset. Reports of subjective cognitive decline are also often present prior to formal diagnosis. Yet, the relationship between LC structural integrity and subjective cognitive decline has remained unexplored. Here, we aimed to explore these potential associations.
We examined 381 community-dwelling men (mean age = 67.58; SD = 2.62) in the Vietnam Era Twin Study of Aging who underwent LC-sensitive magnetic resonance imaging and completed the Everyday Cognition scale to measure subjective cognitive decline along with their selected informants. Mixed models examined the associations between rostral-middle and caudal LC integrity and subjective cognitive decline after adjusting for depressive symptoms, physical morbidities, and family. Models also adjusted for current objective cognitive performance and objective cognitive decline to explore attenuation.
For participant ratings, lower rostral-middle LC contrast to noise ratio (LCCNR) was associated with significantly greater subjective decline in memory, executive function, and visuospatial abilities. For informant ratings, lower rostral-middle LCCNR was associated with significantly greater subjective decline in memory only. Associations remained after adjusting for current objective cognition and objective cognitive decline in respective domains.
Lower rostral-middle LC integrity is associated with greater subjective cognitive decline. Although not explained by objective cognitive performance, such a relationship may explain increased AD risk in people with subjective cognitive decline as the LC is an important neural substrate important for higher order cognitive processing, attention, and arousal and one of the first sites of AD pathology.
Clarifying the relationship between depression symptoms and cardiometabolic and related health could clarify risk factors and treatment targets. The objective of this study was to assess whether depression symptoms in midlife are associated with the subsequent onset of cardiometabolic health problems.
The study sample comprised 787 male twin veterans with polygenic risk score data who participated in the Harvard Twin Study of Substance Abuse (‘baseline’) and the longitudinal Vietnam Era Twin Study of Aging (‘follow-up’). Depression symptoms were assessed at baseline [mean age 41.42 years (s.d. = 2.34)] using the Diagnostic Interview Schedule, Version III, Revised. The onset of eight cardiometabolic conditions (atrial fibrillation, diabetes, erectile dysfunction, hypercholesterolemia, hypertension, myocardial infarction, sleep apnea, and stroke) was assessed via self-reported doctor diagnosis at follow-up [mean age 67.59 years (s.d. = 2.41)].
Total depression symptoms were longitudinally associated with incident diabetes (OR 1.29, 95% CI 1.07–1.57), erectile dysfunction (OR 1.32, 95% CI 1.10–1.59), hypercholesterolemia (OR 1.26, 95% CI 1.04–1.53), and sleep apnea (OR 1.40, 95% CI 1.13–1.74) over 27 years after controlling for age, alcohol consumption, smoking, body mass index, C-reactive protein, and polygenic risk for specific health conditions. In sensitivity analyses that excluded somatic depression symptoms, only the association with sleep apnea remained significant (OR 1.32, 95% CI 1.09–1.60).
A history of depression symptoms by early midlife is associated with an elevated risk for subsequent development of several self-reported health conditions. When isolated, non-somatic depression symptoms are associated with incident self-reported sleep apnea. Depression symptom history may be a predictor or marker of cardiometabolic risk over decades.
Frascati international research criteria for HIV-associated neurocognitive disorders (HAND) are controversial; some investigators have argued that Frascati criteria are too liberal, resulting in a high false positive rate. Meyer et al. recommended more conservative revisions to HAND criteria, including exploring other commonly used methodologies for neurocognitive impairment (NCI) in HIV including the global deficit score (GDS). This study compares NCI classifications by Frascati, Meyer, and GDS methods, in relation to neuroimaging markers of brain integrity in HIV.
Two hundred forty-one people living with HIV (PLWH) without current substance use disorder or severe (confounding) comorbid conditions underwent comprehensive neurocognitive testing and brain structural magnetic resonance imaging and magnetic resonance spectroscopy. Participants were classified using Frascati criteria versus Meyer criteria: concordant unimpaired [Frascati(Un)/Meyer(Un)], concordant impaired [Frascati(Imp)/Meyer(Imp)], or discordant [Frascati(Imp)/Meyer(Un)] which were impaired via Frascati criteria but unimpaired via Meyer criteria. To investigate the GDS versus Meyer criteria, the same groupings were utilized using GDS criteria instead of Frascati criteria.
When examining Frascati versus Meyer criteria, discordant Frascati(Imp)/Meyer(Un) individuals had less cortical gray matter, greater sulcal cerebrospinal fluid volume, and greater evidence of neuroinflammation (i.e., choline) than concordant Frascati(Un)/Meyer(Un) individuals. GDS versus Meyer comparisons indicated that discordant GDS(Imp)/Meyer(Un) individuals had less cortical gray matter and lower levels of energy metabolism (i.e., creatine) than concordant GDS(Un)/Meyer(Un) individuals. In both sets of analyses, the discordant group did not differ from the concordant impaired group on any neuroimaging measure.
The Meyer criteria failed to capture a substantial portion of PLWH with brain abnormalities. These findings support continued use of Frascati or GDS criteria to detect HIV-associated CNS dysfunction.
Understanding the genetic and environmental contributions to measures of brain structure such as surface area and cortical thickness is important for a better understanding of the nature of brain-behavior relationships and changes due to development or disease. Continuous spatial maps of genetic influences on these structural features can contribute to our understanding of regional patterns of heritability, since it remains to be seen whether genetic contributions to brain structure respect the boundaries of any traditional parcellation approaches. Using data from magnetic resonance imaging scans collected on a large sample of monozygotic and dizygotic twins in the Vietnam Era Twin Study of Aging, we created maps of the heritability of areal expansion (a vertex-based area measure) and cortical thickness and examined the degree to which these maps were affected by adjustment for total surface area and mean cortical thickness. We also compared the approach of estimating regional heritability based on the average heritability of vertices within the region to the more traditional region-of-interest (ROI)-based approach. The results suggested high heritability across the cortex for areal expansion and, to a slightly lesser degree, for cortical thickness. There was a great deal of genetic overlap between global and regional measures for surface area, so maps of region-specific genetic influences on surface area revealed more modest heritabilities. There was greater inter-regional variability in heritabilities when calculated using the traditional ROI-based approach compared to summarizing vertex-by-vertex heritabilities within regions. Discrepancies between the approaches were greatest in small regions and tended to be larger for surface area than for cortical thickness measures. Implications regarding brain phenotypes for future genetic association studies are discussed.
The present study aimed to determine how older bilingual
subjects' naming performance is affected by their knowledge of two
languages. Twenty-nine aging (mean age = 74.0; SD = 7.1)
Spanish–English bilinguals were asked to name all pictures in the
Boston Naming Test (BNT) first in their dominant language and then in
their less-dominant language. Bilinguals with similar naming scores in
each language, or relatively balanced bilinguals, named more pictures
correctly when credited for producing a correct name in either language.
Balanced bilinguals also named fewer pictures in their dominant language
than unbalanced bilinguals, and named more pictures correctly in both
languages if the pictures had cognate names (e.g., dart is
dardo in Spanish). Unbalanced bilinguals did not benefit from the
alternative (either-language) scoring procedure and showed cognate effects
only in their nondominant language. These findings may help to guide the
interpretation of neuropsychological data for the purpose of determining
cognitive status in older bilinguals and can be used to develop models of
bilingual language processing. Bilinguals' ability to name pictures
reflects their experience with word forms in both languages.
(JINS, 2007, 13, 197–208.)
We reported that bilingualism affects BNT performance, and that people
who are “more bilingual” show larger “bilingual
effects” on naming. The commentators suggested the interesting
possibilities that degree of bilingualism may not be as critical as
immersion in two different language environments over the course of a
lifetime (Bialystok & Craik, this issue),
and that proficiency in Spanish (or lack thereof in English-dominant
speakers; Acevedo & Lowenstein, this issue)
may be more powerful predictors of the effects we reported. In our
response, we use the literature on bilingualism, and additional
exploratory analyses of the data we published in this issue to predict
that our findings will generalize (a) to bilinguals who speak languages
other than Spanish and English, and perhaps even to (b) English-dominant
bilinguals who were educated in an English speaking environment.
(JINS, 2007, 13, 215–218.)
The very high sensitivity and specificity of odor identification tasks in discriminating between Alzheimer's patients and normals suggests that they reflect the presence of underlying neuropathology. Significant neuropathological changes are seen in areas critical to processing olfactory information, even in the early stages of Alzheimer's disease (AD). The current study was designed to investigate whether performance on olfactory tasks (odor threshold and odor identification) was related to volumetric MRI measures of mesial temporal areas central to olfactory information processing and important in the neuropathology of AD. Participants were 8 male and 5 female patients with probable AD, and 10 male and 12 female normal age-matched controls, diagnosed at the UCSD Alzheimer's Disease Research Center. The study investigated correlations between volumetric measures of hippocampus, the parahippocampal gyrus and the amygdala, and the psychophysical measures of olfactory function. Robust relationships were observed between mesial temporal lobe volumes and olfactory functional measures. The finding of a strong relationship between left hippocampal volume and performance on the odor identification task (r = .85) is compatible with a left-hemisphere superiority for verbally mediated olfactory tasks. The findings suggest a neural substrate for the breakdown in functional performance on verbally mediated odor identification tasks in Alzheimer's disease and suggest the utility of quantitative MRI measures and psychophysical performance in the assessment of AD. These results support the potential clinical utility of inclusion of odor identification tests in diagnostic batteries for detecting AD. (JINS, 2003, 9, 459–471.)
This article presents a new method that can compare lexical priming (word–word) and
sentential priming (sentence–word) directly within a single paradigm. We show that it can
be used to address modular theories of word comprehension, which propose that the effects of
sentence context occur after lexical access has taken place. Although lexical priming and
sentential priming each occur very quickly in time, there should be a brief time window in which
the former is present but the latter is absent. Lexical and sentential priming of unambiguous words
were evaluated together, in competing and converging combinations, using time windows
designed to detect an early stage where lexical priming is observed but sentential priming is not.
Related and unrelated word pairs were presented visually, in rapid succession, within auditory
sentence contexts that were either compatible or incompatible with the target (the second word in
each pair). In lexical decision, the additive effects of lexical priming and sentential priming were
present under all temporal conditions, although the latter was always substantially larger. In
cross-modal naming, sentential priming was present in all temporal conditions; lexical priming was
more fragile, interacting with timing and sentential congruence. No evidence was found for a
stage in which lexical priming is present but sentential priming is absent – a finding that is
difficult to reconcile with two-stage models of lexical versus sentential priming. We conclude that
sentential context operates very early in the process of word recognition, and that it can interact
with lexical priming at the earliest time window.
Fifty-three volunteer participants were studied with
the fade-in task (Ostergaard, 1998) to measure naming
latency, word priming, and recognition-memory performance,
and with morphometric magnetic resonance imaging (MRI)
techniques to measure volumes of mesial temporal lobe,
diencephalic, striatal, and neocortical structures. The
relationship between measures of cerebral volume loss and
performance deficits was modeled using simultaneous regression
analyses in which the behavioral measures were dependent
variables. The results suggested that damage in both hippocampal
and amygdala/entorhinal areas as well as damage in the
diencephalon and the nucleus accumbens all contributed
independently to the severity of recognition-memory deficits.
Both caudate nucleus damage and hippocampal damage contributed
independently to increased naming latency (slowed single-word
reading). Finally, only damage in the hippocampus appeared
to result in decreased word priming. These results provide
further evidence against the assertion that word priming
represents a form of memory unaffected by damage to the
mesial temporal lobes. (JINS, 2001, 7,
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