60 research outputs found
Risk factors for cognitive decline in older people with type 2 diabetes
No full textPeople with type 2 diabetes are at increased risk of age-related cognitive impairment.
Previous literature has focused on case-control studies comparing rates of cognitive
impairment in patients with and without diabetes. Investigations of potential risk
factors for cognitive impairment (including those with increased prevalence in
diabetes, such as macrovascular disease, and diabetes-specific factors such as
hypoglycaemia) in study populations consisting exclusively of patients with type 2
diabetes have been largely neglected. Moreover, previous studies have failed to take
advantage of the extensive characterisation and prospective nature of longitudinal
cohort studies to investigate the relative predictive ability of a wider range of
potential risk factors for cognitive decline. Using data from the prospective
Edinburgh Type 2 Diabetes Study (ET2DS) the present thesis aimed (i) to determine
associations of cognitive decline with macrovascular disease and with severe
hypoglycaemia, and (ii) to compare a wider range of potential risk factors in their
ability to predict cognitive decline.
In 2006/2007, 1066 patients with type 2 diabetes (aged 60 to 75 years) attended the
baseline ET2DS clinic and 831 returned for the follow-up at year 4. Subjects were
extensively characterised for risk factor profiles at baseline, and at year 4 for
incidence of severe hypoglycaemia. Socioeconomic status was estimated using
postcode data. Scores on seven tests of age-sensitive ‘fluid’ cognitive function,
which were administered at baseline and at year 4, were used to derive a general
cognitive component (‘g’). A vocabulary-based test, administered at baseline,
estimated pre-morbid ability. Findings are reported in three parts. 1.) Macrovascular
disease and cognition: Subjects with higher levels of biomarkers indicative of
subclinical macrovascular disease, including plasma N-terminal pro-brain natriuretic
peptide and carotid intima-media thickness, had significantly steeper four-year
cognitive decline, independent of traditional cardiovascular risk factors, stroke,
socioeconomic status and estimated pre-morbid cognitive ability. For ankle-brachial
pressure index, the association fell just short of statistical significance. Effect sizes
were overall modest, with fully adjusted standardised beta coefficients ranging from
0.06 to -0.12. Little evidence was found for associations of the symptomatic markers
of macrovascular disease with four-year change in cognitive function that was independent of participants’ pre-morbid ability and socioeconomic status. 2.) Severe
hypoglycaemia and cognition: Subjects with lower cognitive ability at baseline were
at two-fold increased risk of experiencing their first-ever incident severe
hypoglycaemia during follow-up. The rate of four-year cognitive decline was
significantly steeper in those exposed to hypoglycaemia compared with
hypoglycaemia-free participants, independently of cardiovascular risk factors, microand
macrovascular disease and of estimated pre-morbid cognitive ability. Effect sizes
again were overall modest (Cohen’s d = 0.2 to 0.3 for statistically significant
differences in four-year cognitive decline between subjects with and those without
hypoglycaemia, following multivariable adjustment) 3.) Consideration of a wider
range of risk factors and cognition: A stepwise linear regression model including a
total of 15 metabolic and vascular risk factors identified inflammation, smoking and
poorer glycaemic control (in addition to some of the subclinical markers of
macrovascular disease) as predictive of a steeper four-year cognitive decline. Other
traditional cardiovascular risk factors, diabetic retinopathy, clinical macrovascular
disease and a baseline history of severe hypoglycaemia were not included in this
model. The interpretation of the latter finding is limited, however, by the fact that the
stepwise regression procedure may exclude true predictors from a model when they
correlate with already included risk factors.
This thesis has demonstrated associations of later-life cognitive decline in people
with type 2 diabetes with markers of subclinical macrovascular disease and poor
glycaemic control (including hypoglycaemia) as well as other cardiometabolic risk
factors (inflammation, smoking). Findings suggest that associations are relatively
weak and complex due to inter-relationships amongst risk factors, and indicate a role
of pre-morbid ability and socioeconomic status (which as risk factors are difficult to
modify) in the relationships of risk factors with cognitive decline. Future research
including case-control studies to compare risk factor associations between people
with type 2 diabetes and non-diabetic older adults and randomised controlled trials to
evaluate potential causal effects of individual modifiable risk factors on cognitive
decline, will help to evaluate the mechanisms underlying the observation that people
with type 2 diabetes are at risk of cognitive impairment in later life
Post-Operative Cognitive Impairment: A Cognitive Epidemiology Perspective
No full textCognitive epidemiology investigates cognitive predictors of health and disease outcomes. Post-operative cognitive impairment is a common complication of surgery but has been neglected as a health outcome in cognitive epidemiology research. This is despite the fact that knowledge of cognitive predictors of post-operative cognitive impairment can be utilized for risk stratification, informed decision-making (in elective surgery), and personalized care of patients during the postoperative period. In this narrative review, the current literature on cognitive predictors of post-operative cognitive impairment and gaps therein are summarized
Hypotheses
No full textWe hypothesize that i) plasma amyloid correlates with CSF amyloid and ii) plasma amyloid correlates with cognitive function/cognitive declin
Metabolische Risikofaktoren für kognitive Dysfunktion im perioperativen Verlauf
No full textPostoperative cognitive dysfunction (POCD) is characterized by a cognitive decline from pre- to post-surgery assessment, but is underresearched from an epidemiological perspective. Previous studies have identified metabolic dysfunction as a risk factor for age-related cognitive impairment (ACI) which too is characterized by cognitive deficits but occurs in the general population during ageing. Thus, metabolic dysfunction is a strong candidate risk factor for POCD. Here, I used a total of 4 surgical cohort studies of middle-aged to older adults with extensive anthropometric, clinical (and in part molecular) phenotyping as well as detailed pre- and post-surgical cognitive assessment to test the hypothesis that ACI and POCD share metabolic risk factors. I found partial evidence for in favor of this hypothesis. The implications of this work are three-fold: i) the findings suggest that ACI and POCD may (in part) be driven by similar pathophysiological mechanisms. ii) by measuring metabolic function before surgery, we may be able to risk stratify older surgical patients and – in elective surgery settings – empower at-risk patients for informed decision making. ii) if future work determines that the associations found here reflect causal relationships of metabolic dysfunction with ACI and POCD, we could set up preventive measures. Ultimately, the epidemiological analyses presented here provide one step towards a better understanding of ACI and POCD
Expertimental design
No full textThe study combines 2 samples of older people (age >64 years) recruited at a) a local memory clinic and b) a local hospital. Study design is cross-sectional for a) and cross-sectional/prospective for b)
Replication of a diagnostic tool to measure beta amyloid in plasma as a marker of cognitive impairment
No full textCognitive impairment is a disabling consequence of aging and a significant diagnosis impacting the lives of older adults. To date, beta amyloid measured in cerebrospinal fluid (CSF) has been a reliable diagnostic tool for cognitive impairment in the context of Alzheimer´s Disease (AD) and thus has become the gold standard in clinical practice. Repeat attempts to measure beta amyloid from blood, which is less invasive and cheaper compared with CSF, have proven unsuccessful. Here, we plan to determine the validity of a new measurement technique that determines amyloid in plasma using samples of older adults that span cognitively normal to cognitively impaired individuals
Experimental design
No full textThe study combines 2 samples of older people (aged at least 65 years) recruited at a) a local memory clinic ("Study 1"; N=100) and b) a local Hospital ("Study 2"; N=200). Participants in Study 2 undergo surgery and were cognitively tested before and 3 months after surgery. Analyses are thus cross-sectional for Study 1 and cross-sectional/prospective for Study 2
Analysis plan
No full textFollowing Initial descriptive analyses, study 1 will be used to determine associations of plasma amyloid with amyloid in cerebrospinal fluid. Associations of plasma amyloid with cognitive test performance will then be determined in study 1 and study 2. Finally, for study 2, associations of plasma amyloid with cognitive decline 3 months after surgery will be explored.
Thus each study will be analyzed separately though results will be compared between the 2 studies following project completion
Scoping Review Protocol
No full textScoping Review of Health Status, Health Behaviour and Subjective Stress Perception of Nursing Staff in Germany: A Protocol for Implementatio
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