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• W2904065877 abstract "The last 10–20 years have seen a rapid expansion in population-based cohort studies reporting on risk factors for dementia. Whilst the largest and longest-running of these were generally set up for other outcomes originally (e.g. cardiovascular endpoints), there are a growing number of cohort studies specifically created for investigating dementia. Aside from the wealth of findings on cardiovascular or other physical health risk factors, and on sociodemographic risk factors already well-recognised (e.g. age, gender, education), probably the most studied exposure for dementia risk has been prior mental health. This in turn perhaps stems from researchers' clinical experience of people presenting initially with functional mental disorders in whom dementia becomes evident at a later date, and the natural curiosity concerning whether this is more than coincidence. In what is now a substantial body of well-conducted prospective research, associations between affective distress/disorders and increased dementia risk are commonly and fairly consistently reported. Most of these findings are for depression or depressive symptoms, although they extend to associations with midlife psychological distress (1, 2), and with negative affect or proneness to psychological distress as personality traits 3, 4. As concluded in a 2016 systematic review 5, people reporting anxiety symptoms have also been found to have a higher risk of subsequent dementia, and this is supported by evidence from more recent reports 6, 7, although previous investigations have tended to ascertain anxiety from scores on screening scales. The study reported by Santabárbara and colleagues in this issue 8 has the advantage of using a more in-depth schedule for mental health symptoms and an accompanying algorithm in wide use which seeks to identify and distinguish clinically significant anxiety disorder, amongst other disorders. Their findings, of higher dementia incidence in people with case-level anxiety disorder, therefore have higher potential relevance (than those derived from screening scale cut-offs) for clinicians treating people with late-life anxiety disorders. However, although the key dementia risk associations were found to be independent of depression in this study, it would be premature to assume a specific role of anxiety because the two disorders are so closely interrelated. Given findings from other studies, the observed association might well reflect one with affective symptoms/disorders as a whole, although further investigation of risk symptom profiles would be helpful. For example, depressive and anxiety symptoms have been found to show different patterns of association with mortality as an outcome 9 and different associations with IQ as an exposure 10 in general population samples, despite being highly aetiologically related. The question of causality is routinely challenging for studies of dementia risk factors with similar durations of follow-up to the study here (e.g. <10 years), because of the well-recognised long periods over which the pathologies underlying disorders such as Alzheimer's disease develop. For studies of depression or anxiety as risk factors for dementia, it remains quite possible that at least some of the observed associations reflect affective symptoms occurring as part of the dementia prodrome, before cognitive impairment is sufficiently severe to be noticeable or causing difficulties. This might involve a simple reaction to early difficulties experienced with memory and/or other cognitive functions, although many studies (including that of Santabárbara and colleagues) have not found any/much effect of adjusting for self-reported cognitive decline. Instead, it seems more likely that prodromal affective symptoms, if present, arise as a direct consequence of the neurodegenerative process even in people who have not apparently noticed any difficulties with cognitive function. However, an alternative possibility is that affective disorders, whether anxiety or depressive, might directly act as risk factors for dementia, or might reflect another underlying causal process. This is clearly important because of the potential for risk modification through intervention, but the challenge remains of how to demonstrate this risk effect. Distinguishing risk and prodromal factors is notoriously problematic when risk factors are measured within the period where neurodegeneration is significant enough to cause symptoms. It is much easier to assume causation when the risk factor is measured 10 or 20 years previously. However, it would be surprising if dementia risk was determined entirely by midlife, and there is no reason to suppose that at least some risk factors for dementia may act much closer to the point of clinical onset, despite the inconvenience to researchers attempting to demonstrate shorter-term effects. The lack of association found between anxiety (symptoms or disorder) and dementia incidence in the Rotterdam Study stands out as an important negative finding in a large and well-characterised cohort 11; however, the long duration of follow-up in that analysis might have obscured associations if associations with anxiety are shorter-term and obscured by other factors over longer periods. The question of causality naturally receives consideration by Santabárbara and colleagues in their discussion of findings. This author is not convinced that the exclusion of dementia ‘subcases’ can be guaranteed in this study, because cognitive items in the Geriatric Mental State (GMS) schedule are relatively imprecise and largely confined to orientation tests; therefore, it is possible that some of the participants at baseline might have had early impairment. The differences in risk associations between subcases and cases of anxiety disorder are more persuasive, since it seems likely that prodromal symptoms would manifest more equally across affective disorder severity (i.e. predicting similar dementia hazard ratios between cases and subcases of anxiety disorder) unless there was a process whereby anxiety symptoms worsened and became more ‘case-like’ as dementia onset approached. On the other hand, if anxiety symptoms were acting as risk factors for dementia then it would be expected for the hazard ratios to increase with increasing severity of the anxiety syndrome, as it does in the cohort described by Santabárbara. Ultimately observational data are always going to fall short of providing conclusive proof for causation, and dementia is unfortunately a condition where causation, whether involving biological or social processes, only really becomes demonstrable when modifiers of assumed causal processes are put to the test in randomised controlled trials. Thus, the role of cholinergic signalling in dementia-associated cognitive impairment (a lot more limited than originally expected) was only really clarified when acetyl cholinesterase inhibitors were evaluated, and the causal roles of beta-amyloid and other neuropathological pathways have still to be demonstrated despite very substantial funding of so-far-unsuccessful intervention trials to date. The clear question arising from associations between affective disorders and dementia risk is the extent to which the outcome might be reduced through modification of the exposure. However, the 346 person years of follow-up of 91 cases of anxiety disorder in the study by Santabárbara and colleagues gave rise to only 7 cases of dementia and an intervention in the same number of people, and sustained over the same follow-up, would be expected to prevent only 4 to 5 cases if risks were reduced to the same level as in those with no anxiety (i.e. an optimistic target for anxiolytic intervention, whether pharmacological or psychotherapeutic). This makes for a very large number needed to treat. A trial with biomarker-measured endpoints might be more feasible; however, substantially more knowledge would be required of how anxiety disorder might influence risk and therefore what biomarkers would be an appropriate choice for intervention evaluation. The study by Santabárbara and colleagues illustrates many of the challenges inherent in dementia risk factor research, including the long periods during which significant neuropathology is likely to be present and exerting influences on apparent ‘risk profiles’, as well as the practical difficulties of carrying out trials with dementia incidence as the primary outcome. On the other hand, the results can be seen as encouraging for clinical populations: despite the 2- to 3-fold increased risk of dementia observed in people with suspected anxiety disorder, the actual levels of risk (approximately 2% per year) remained low over a reasonable duration of follow-up. This is perhaps a more hopeful message for people with late-life anxiety disorders, and those providing treatment, than the age-old frustrations for academics of unpicking cause and effect in dementia research. None declared." @default.
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• W2904065877 date "2018-12-18" @default.
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• W2904065877 title "Anxiety and dementia: cause or effect?" @default.
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