Incidence Of Dementia In People Research Articles

Risk of Dementia in Patients with Diabetes Using Sodium-Glucose Transporter2 Inhibitors (SGLT2i): A Systematic Review, Meta-Analysis, and Meta-Regression.

Dementia is quite prevalent and among the leading causes of death worldwide. According to earlier research, diabetes may increase the possibility of developing dementia. However, the association between antidiabetic agents and dementia is not yet clear. This investigation examines the association between the use of sodium-glucose transporter2 inhibitors (SGLT2i) and the risk of dementia in patients with diabetes. Up to April 18, 2023, four databases-Europe PMC, Medline, Scopus, and Cochrane Library-were searched for relevant literature. We included all studies that examine dementia risk in adults with diabetes who use SGLT2i. Random-effect models were used to compute the outcomes in this investigation, producing pooled odds ratios (OR) with 95% confidence intervals (CI). Pooled data from seven observational studies revealed that SGLT2i use was linked to a lower risk of dementia in people with diabetes (OR 0.45, 95%CI 0.34-0.61; p < 0.00001, I2 = 97%). The reduction in the risk of dementia due to SGLT2i's neuroprotective effect was only significantly affected by dyslipidemia (p = 0.0004), but not by sample size (p = 0.2954), study duration (p = 0.0908), age (p = 0.0805), sex (p = 0.5058), hypertension (p = 0.0609), cardiovascular disease (p = 0.1619), or stroke (p = 0.2734). According to this research, taking SGLT2i reduces the incidence of dementia in people with diabetes by having a beneficial neuroprotective impact. Randomized controlled trials (RCTs) are still required in order to verify the findings of our research.

Incidence and risk of dementia in people with Anxiety over 50 years old – an electronic health records study

AbstractBackgroundDepression is a well‐established risk factor for dementia, but we know far less about the links between Anxiety and future dementia risk in older people. The aim was therefore to investigate the incidence of dementia in people with and without Anxiety above the age of 50 years over a 10‐year period.MethodThe Health Improvement Network (THIN) was used, a large UK primary care dataset, that includes approximately 15.6 million patients, which is representative of the UK population. All people between 1st January 2008 and 31 December 2018 who had new onset Anxiety over the age of 50 years were identified. At the time of the first record of Anxiety, each person was individually matched to 4 unexposed persons based on their sex and age and Exposure Density Sampling was used, creating a dynamic cohort. Weibull survival regression models were fitted and hazard ratios (HR) were estimated for modelling time‐to‐dementia in those with and without Anxiety; and when determining the risk of developing dementia in those with Anxiety. Hazard ratio estimates were adjusted for sociodemographic and lifestyle factors, and relevant physical and mental health conditions.ResultIn this cohort study, there were 37,824 men and 68,761 women diagnosed with a first episode of Anxiety. Of those who had Anxiety, 2,792 people developed dementia during the follow up period, compared to 19,000 people in the non‐Anxiety group. The incidence of dementia in those with and without Anxiety was 7.21 (95% CI 6.94‐7.48) and 3.22 (95% CI 3.18‐3.28) respectively per 1,000 person‐years. The risk of dementia was increased 2.47‐fold [HR 2.47 (CI 2.37‐ 2.57)] in the Anxiety group when compared to the non‐Anxiety group after adjustment for age, sex, social deprivation, alcohol, smoking, BMI, diabetes mellitus, cardiovascular diseases, learning disabilities, HIV, multiple sclerosis, brain injury and hearing impairment.ConclusionThe incidence of dementia was greater in those with Anxiety and the risk of developing dementia was more than doubled in people with Anxiety compared to those without. This provides further evidence that Anxiety is a potential risk factor for dementia.

Trends in the incidence of dementia in people with hypertension in the UK 2000 to 2021.

We investigated trends in the incidence of dementia in UK adults with hypertension. Primary care electronic health records from IQVIA Medical Research Data UK, previously known as THIN, were used to identify 2,133,118 adults aged ≥40 years with hypertension over 2000 to 2021. The annual incidence rate and average annual percentage change in recorded dementia diagnoses were estimated and stratified by sex, 10-year age bands, Townsend deprivation quintiles and dementia subtype. The crude incidence rate of dementia in people with hypertension increased from 1.98 (95% confidence internal [CI] 1.89-2.07) per 1000 person-years at risk (PYAR) in 2000 to 5.29 per 1000 PYAR (95% CI 5.07-5.53) in 2021, corresponding to an average annual increase of 4.1% (95% CI 3.3-5.0). Those aged ≥80 years, the most economically deprived (Townsend=5), and Alzheimer's disease subtype reported the highest incidence rate within their respective categories. The annual incidence rate of dementia in the hypertensive population has increased over the last 22 years. New dementia diagnosis in the hypertensive population has increased over 22 years.The Alzheimer's disease subtype reported the highest incidence rate in people with hypertension.Difference in dementia incidence between hypertensive females and males has reduced.Difference in dementia incidence among deprivation categories has reduced in recent years.

Socioeconomic, Behavioral and Clinical Characteristics and Risk of Depression and Dementia Comorbidity: A Prospective Cohort Study

Background: Depressive symptom may be a risk factor or prodrome of dementia, and the two neuropsychiatric disorders are commonly comorbid in late-life, but the patterns of depression-dementia comorbidity have not been well established. The current study aimed to investigate the associations of socioeconomic status, behavioral factors and clinical characteristics with the risk of depression-dementia comorbidity, along with how these factors modify the temporal progression of dementia after the onset of depression. Methods: Our analysis was based on data from the ongoing UK Biobank study, which included 497,533 participants (age 37-73 years) between 2006 and 2010, and thereafter followed up to 2020. Three sets of risk factors were assessed at baseline, each on a 5-point scale: socioeconomic status (Townsend deprivation index), behavioral factors (smoking, alcohol consumption, diet, physical activity) and clinical profile (obesity, hypertension, hyperglycemia, hypercholesterolemia). Electronic health records were used to assess the incidence of depression, dementia and comorbidity. Multistate models to estimate the transition-specific hazard ratios (HRs) and 95% confidence interval (CIs) of 3 risk factor scales in the transitions from a healthy state to progression of depression and subsequent comorbid dementia. Findings: During a median follow-up of 11.8 years, 23,516 (4.7%) and 6,872 (1.4%) participants separately developed depression and dementia, 1,341 (0.3%) had depression-dementia comorbidity. Adverse socioeconomic status, behavioral factors and clinical scale was strongly associated with increased risk of depression-dementia comorbidity, with highest vs. lowest group HRs of 2.40 (95% CI: 2.03-2.84), 3.43 (95% CI: 2.35-5.00) and 2.95 (95% CI: 2.06-4.22), respectively. In multistate models, adverse socioeconomic status (HR = 1.35, 95% CI: 1.11-1.65), behavioral factors (HR = 1.85, 95% CI: 1.22-2.80) and clinical scale (HR = 1.75, 95% CI: 1.15-2.66) was significantly associated with elevated risk of transition from depression to comorbid dementia. The incidence of dementia in people with depression was far more than those who were free of depression (9.16 vs. 1.04 per 1000 person-years). Of the 3 risk factor scales, behavioral factors were the strongest predictor of incident dementia whether in those with depression or not. Interpretation: Adverse socioeconomic status, behavioral factors and clinical characteristics increase the risk of depression-dementia comorbidity. Behavioral scale had the strongest association with temporal progression of dementia after the onset of depression, making it a central target for improving healthy aging. Funding: The National Natural Science Foundation of China (71910107004, 91746205). Declaration of Interest: The authors declare that they have no competing interests. Ethical Approval: All participants gave written informed consent prior data collection.UK Biobank has full ethical approval from the NHS National Research Ethics Service (16/NW/0274).

Souvenaid for Alzheimer's disease.

Souvenaid is a dietary supplement with a patented composition (Fortasyn Connect™)which is intended to be used by people with Alzheimer's disease (AD). It has been designed to support the formation and function of synapses in the brain, which are thought to be strongly correlated with cognitive function. If effective, it might improve symptoms of Alzheimer's disease and also prevent the progression from prodromal Alzheimer's disease to dementia. We sought in this review to examine the evidence for this proposition. To assess the effects of Souvenaid on incidence of dementia, cognition, functional performance, and safety in people with Alzheimer's disease. We searched ALOIS, i.e. the specialised register of the Cochrane Dementia and Cognitive Improvement Group, MEDLINE (Ovid SP), Embase (Ovid SP), PsycINFO (Ovid SP), Web of Science (ISI Web of Science), Cinahl (EBSCOhost), Lilacs (BIREME), and clinical trials registries up to 24 June 2020. We also reviewed citations of reference lists of landmark papers, reviews, and included studies for additional studies and assessed their suitability for inclusion in the review. We included randomised, placebo-controlled trials which evaluated Souvenaid in people diagnosed with mild cognitive impairment (MCI) due to AD (also termed prodromal AD) or with dementia due to AD, and with a treatment duration of at least 16 weeks. Our primary outcome measures were incidence of dementia, global and specific cognitive function, functional performance, combined cognitive-functional outcomes and adverse events. We selected studies, extracted data, assessed the quality of trials and intended to conduct meta-analyses according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. We present all outcomes grouped by stage of AD. We included three randomised, placebo-controlled trials investigating Souvenaid in 1097 community-dwelling participants with Alzheimer's disease. One study each included participants with prodromal AD, mild AD dementia and mild-to-moderate AD dementia. We rated the risks of bias of all trials as low. One study (in prodromal AD) was funded by European grants. The other two studies were funded by the manufacturer of Souvenaid. One trial investigated the incidence of dementia in people with prodromal AD at baseline, and found little to no difference between the Souvenaid group and the placebo group after 24 months (RR 1.09, 95% CI 0.82 to 1.43; 1 trial, 311 participants; moderate quality of evidence). In prodromal AD, and in mildand mild-to-moderate Alzheimer's disease dementia, Souvenaid probably results in little or no difference in global or specific cognitive functions (moderate quality of evidence). Everyday function, or the ability to perform activities of daily living, were measured in mild and mild-to-moderate AD dementia. Neither study found evidence of a difference between the groups after 24 weeks of treatment (moderate quality of evidence). Two studies investigated combined cognitive-functional outcomes with the Clinical Dementia Rating Sum of Boxes and observed conflicting results. Souvenaid probably results in slight improvement, which is below estimates of meaningful change, in participants with prodromal Alzheimer's disease after 24 months (moderate quality of evidence), but probably has little to no effect in mild-to-moderate Alzheimer's disease dementia after 24 weeks (moderate quality of evidence). Adverse effects observed were low in all trials, and the available data were insufficient to determine any connection with Souvenaid. Two years of treatment with Souvenaid probably does not reduce the risk of progression to dementia in people with prodromal AD. There is no convincing evidence that Souvenaid affects other outcomes important to people with AD in the prodromal stage or mild-to-moderate stages of dementia. Conflicting evidence on combined cognitive-functional outcomes in prodromal AD and mild AD dementia warrants further investigation. Adverse effects of Souvenaid seem to be uncommon, but the evidence synthesised in this review does not permit us to make a definitive statement on the long-term tolerability of Souvenaid. The effects of Souvenaid in more severe AD dementia or in people with AD at risk of nutritional deficiencies remain unclear.

Effective interventions for potentially modifiable dementia risk factors: Their costs and cost‐effectiveness

AbstractBackgroundThe potential economic value of interventions to prevent dementia is unknown. We modelled this for potentially modifiable dementia risk factors.MethodWe searched PubMed and Web of Science from inception to July 2018 and included interventions that (a) successfully targeted any of nine pre‐specified potentially modifiable risk factors (hypertension, diabetes, hearing loss, obesity, physical inactivity, social isolation, depression, cigarette smoking and less childhood education), (b) had robust evidence that the intervention improved risk or risk behaviour and (c) are feasible in an adult population. We established when in the life‐course each intervention would be delivered. We calculated dementia incidence reduction from: annual incidence of dementia in people with each risk factor; population attributable fraction for each risk, corrected for risk factor clustering, and how effectively the intervention controls the risk factor. We calculated the discounted value of lifetime health gain (including reduced dementia mortality) and impact on cost (including NHS, social care and carer costs) per person eligible for treatment. We estimated annual total expenditure on the fully operational intervention programme in England.ResultWe found effective treatments for hypertension, stopping smoking, diabetes prevention and hearing loss. Treatments for stopping smoking and provision of hearing aids reduced cost. Treatment of hypertension was cost‐effective by reference to standard UK thresholds. The three interventions when fully implemented would save £1·863 billion annually in England, reduce dementia prevalence by 8·5% and produce QALY gains. The intervention for diabetes was unlikely to be cost‐effective in terms of impact on dementia alone.ConclusionThere is a strong case for implementing the three effective interventions on grounds of cost‐effectiveness and quality of life gains, as well as for improvements in general health. While some people will decline or discontinue interventions, there is considerable room for the interventions to remain cost‐saving or cost‐effective even if adherence is lower.

Effective interventions for potentially modifiable risk factors for late-onset dementia: a costs and cost-effectiveness modelling study

The potential economic value of interventions to prevent late-onset dementia is unknown. We modelled this for potentially modifiable risk factors for dementia. For this modelling study, we searched PubMed and Web of Science from inception to March 12, 2020, and included interventions that: successfully targeted any of nine prespecified potentially modifiable risk factors (hypertension, diabetes, hearing loss, obesity, physical inactivity, social isolation, depression, cigarette smoking, and less childhood education); had robust evidence that the intervention improved risk or risk behaviour; and are feasible to enact in an adult population. We established when in the life course each intervention would be delivered. We calculated dementia incidence reduction from annual incidence of dementia in people with each risk factor, and population attributable fraction for each risk, corrected for risk factor clustering, and how effectively the intervention controls the risk factor. We calculated the discounted value of lifetime health gain and effect on cost (including NHS, social care and carer costs) per person eligible for treatment. We estimated annual total expenditure on the fully operational intervention programme in England. We found effective interventions for hypertension, smoking cessation, diabetes prevention, and hearing loss. Treatments for stopping smoking and provision of hearing aids reduced cost. Treatment of hypertension was cost-effective by reference to standard UK thresholds. The three interventions when fully implemented would save £1·863 billion annually in England, reduce dementia prevalence by 8·5%, and produce quality-adjusted life-year gains. The intervention for diabetes was unlikely to be cost-effective in terms of effect on dementia alone. There is a strong case for implementing the three effective interventions on grounds of cost-effectiveness and quality-of-life gains, as well as for improvements in general health. The interventions have the potential to remain cost-saving or cost-effective even with variations in dementia incidence and costs and effectiveness of interventions. Economic and Social Research Council.

Prevalence and Incidence of Dementia in People with Diabetes Mellitus.

Few studies have shown that an increased risk of dementia is associated with diabetes mellitus. To estimate the prevalence and incidence of dementia in people with diabetes in primary care in the UK. We conducted a descriptive study using the UK The Health Improvement Network (THIN) database. People diagnosed with diabetes from 2000 to 2016 were included in the study. Prevalence and incidence rates of dementia were calculated annually, stratified by age and gender. The prevalence of dementia was 0.424% [95% CI (0.420%-0.427%)] in 2000 and 2.508% [95% CI (2.501%-2.515%)] in 2016. The highest prevalence was in those aged 85+ from 2.9% [95% CI (2.890%-2.974%)] in 2000 to 11.3% [95% CI (11.285%-11.384%)] in 2016. The incidence of dementia increased 3.7 times, from 0.181 cases per 100 persons [95% CI (0.179-0.183)] in 2000 to 0.683 cases per 100 persons [95% CI (0.679-0.686)] in 2016, respectively. Women had a higher prevalence and incidence of dementia than men 3.138% [95% CI (3.127%-3.150%)] versus 2.014% [95% CI (2.006%-2.022%)] and 0.820 [95% CI (0.814-0.826)] versus 0.576 cases per 100 persons [95% CI (0.571-0.580)] in 2016, respectively. There was a trend of increasing prevalence and incidence of dementia in people with diabetes over the period of 2000 to 2016. This study adds to the evidence on dementia prevalence and incidence, particularly in the diabetic population.

Does electroconvulsive therapy cause brain damage: An update.

Electroconvulsive therapy (ECT) is an effective modality of treatment for a variety of psychiatric disorders. However, it has always been accused of being a coercive, unethical, and dangerous modality of treatment. The dangerousness of ECT has been mainly attributed to its claimed ability to cause brain damage. This narrative review aims to provide an update of the evidence with regard to whether the practice of ECT is associated with damage to the brain. An accepted definition of brain damage remains elusive. There are also ethical and technical problems in designing studies that look at this question specifically. Thus, even though there are newer technological tools and innovations, any review attempting to answer this question would have to take recourse to indirect methods. These include structural, functional, and metabolic neuroimaging; body fluid biochemical marker studies; and follow-up studies of cognitive impairment and incidence of dementia in people who have received ECT among others. The review of literature and present evidence suggests that ECT has a demonstrable impact on the structure and function of the brain. However, there is a lack of evidence at present to suggest that ECT causes brain damage.

Vitamin and mineral supplementation for preventing dementia or delaying cognitive decline in people with mild cognitive impairment.

Vitamins and minerals have many functions in the nervous system which are important for brain health. It has been suggested that various different vitamin and mineral supplements might be useful in maintaining cognitive function and delaying the onset of dementia. In this review, we sought to examine the evidence for this in people who already had mild cognitive impairment (MCI). To evaluate the effects of vitamin and mineral supplementation on cognitive function and the incidence of dementia in people with mild cognitive impairment. We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group's (CDCIG) specialised register, as well as MEDLINE, Embase, PsycINFO, CENTRAL, CINAHL, LILACs, Web of Science Core Collection, ClinicalTrials.gov, and the WHO Portal/ICTRP, from inception to 25 January 2018. We included randomised or quasi-randomised, placebo-controlled trials which evaluated orally administered vitamin or mineral supplements in participants with a diagnosis of mild cognitive impairment and which assessed the incidence of dementia or cognitive outcomes, or both. We were interested in studies applicable to the general population of older people and therefore excluded studies in which participants had severe vitamin or mineral deficiencies. We sought data on our primary outcomes of dementia incidence and overall cognitive function and on secondary outcomes of episodic memory, executive function, speed of processing, quality of life, functional performance, clinical global impression, adverse events, and mortality. We conducted data collection and analysis according to standard Cochrane systematic review methods. We assessed the risk of bias of included studies using the Cochrane 'Risk of bias' assessment tool. We grouped vitamins and minerals according to their putative mechanism of action and, where we considered it to be clinically appropriate, we pooled data using random-effects methods. We used GRADE methods to assess the overall quality of evidence for each comparison and outcome. We included five trials with 879 participants which investigated B vitamin supplements. In four trials, the intervention was a combination of vitamins B6, B12, and folic acid; in one, it was folic acid only. Doses varied. We considered there to be some risks of performance and attrition bias and of selective outcome reporting among these trials. Our primary efficacy outcomes were the incidence of dementia and scores on measures of overall cognitive function. None of the trials reported the incidence of dementia and the evidence on overall cognitive function was of very low-quality. There was probably little or no effect of B vitamins taken for six to 24 months on episodic memory, executive function, speed of processing, or quality of life. The evidence on our other secondary clinical outcomes, including harms, was very sparse or very low-quality. There was evidence from one study that there may be a slower rate of brain atrophy over two years in participants taking B vitamins. The same study reported subgroup analyses based on the level of serum homocysteine (tHcy) at baseline and found evidence that B vitamins may improve episodic memory in those with tHcy above the median at baseline.We included one trial (n = 516) of vitamin E supplementation. Vitamin E was given as 1000 IU of alpha-tocopherol twice daily. We considered this trial to be at risk of attrition and selective reporting bias. There was probably no effect of vitamin E on the probability of progression from MCI to Alzheimer's dementia over three years (HR 1.02; 95% CI 0.74 to 1.41; n = 516; 1 study, moderate-quality evidence). There was also no evidence of an effect at intermediate time points. The available data did not allow us to conduct analyses, but the authors reported no significant effect of three years of supplementation with vitamin E on overall cognitive function, episodic memory, speed of processing, clinical global impression, functional performance, adverse events, or mortality (five deaths in each group). We considered this to be low-quality evidence.We included one trial (n = 256) of combined vitamin E and vitamin C supplementation and one trial (n = 26) of supplementation with chromium picolinate. In both cases, there was a single eligible cognitive outcome, but we considered the evidence to be very low-quality and so could not be sure of any effects. The evidence on vitamin and mineral supplements as treatments for MCI is very limited. Three years of treatment with high-dose vitamin E probably does not reduce the risk of progression to dementia, but we have no data on this outcome for other supplements. Only B vitamins have been assessed in more than one RCT. There is no evidence for beneficial effects on cognition of supplementation with B vitamins for six to 24 months. Evidence from a single study of a reduced rate of brain atrophy in participants taking vitamin B and a beneficial effect of vitamin B on episodic memory in those with higher tHcy at baseline warrants attempted replication.

Primary and secondary prevention interventions for cognitive decline and dementia - An overview

Dementia is a syndrome characterised by deterioration in memory, thinking, behaviour, and the ability to perform everyday activities, which ultimately may lead to total dependence and death. Since the world’s population is steadily growing older, the number of people with dementia is also increasing. It is therefore of utmost importance to identify effective strategies to prevent or delay its onset.The key findings of this overview of reviews are based on evidence from eight systematic reviews. The results for the single interventions targeting cognitively healthy people suggest that compared to controls: Antihypertensive drugs may lead to a slight decrease in incidence of dementia in people with hypertension (low certainty of evidence). Statin therapy probably leads to little or no difference on incidence of dementia in people with, or at risk of, cardiovascular disease (moderate certainty). Omega-3 Fatty Acids (FAs) probably lead to little or no effect on cognitive test scores (moderate to high certainty). Computerised cognitive training probably leads to a slight improvement in cognitive test scores directly after the training (moderate certainty). Aerobic exercise may lead to little or no effect on cognitive test scores (low certainty). The results for the interventions targeting people with mild cognitive impairment suggest that compared to control: Cholinesterase inhibitors probably lead to a slight decrease in dementia incidence, but to significantly more adverse events (moderate certainty). Vitamin E probably leads to little or no difference in incidence of Alzheimer’s dementia (moderate certainty). Omega-3 FAs probably lead to little or no difference in cognitive test scores (moderate to high certainty). We did not find any reviews that evaluated the effects of interventions targeting more than one risk factor, and we can therefore not say anything about the combined effects of these interventions.

Souvenaid for Alzheimer's disease

Background Souvenaid is a dietary supplement with a patented composition (Fortasyn Connect™)which is intended to be used by people with Alzheimer's disease (AD). It has been designed to support the formation and function of synapses in the brain, which are thought to be strongly correlated with cognitive function. If effective, it might improve symptoms of Alzheimer's disease and also prevent the progression from prodromal Alzheimer's disease to dementia. We sought in this review to examine the evidence for this proposition. Objectives To assess the effects of Souvenaid on incidence of dementia, cognition, functional performance, and safety in people with Alzheimer's disease. Search methods We searched ALOIS, i.e. the specialised register of the Cochrane Dementia and Cognitive Improvement Group, MEDLINE (Ovid SP), Embase (Ovid SP), PsycINFO (Ovid SP), Web of Science (ISI Web of Science), Cinahl (EBSCOhost), Lilacs (BIREME), and clinical trials registries up to 24 June 2020. We also reviewed citations of reference lists of landmark papers, reviews, and included studies for additional studies and assessed their suitability for inclusion in the review. Selection criteria We included randomised, placebo-controlled trials which evaluated Souvenaid in people diagnosed with mild cognitive impairment (MCI) due to AD (also termed prodromal AD) or with dementia due to AD, and with a treatment duration of at least 16 weeks. Data collection and analysis Our primary outcome measures were incidence of dementia, global and specific cognitive function, functional performance, combined cognitive-functional outcomes and adverse events. We selected studies, extracted data, assessed the quality of trials and intended to conduct meta-analyses according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. We present all outcomes grouped by stage of AD. Main results We included three randomised, placebo-controlled trials investigating Souvenaid in 1097 community-dwelling participants with Alzheimer's disease. One study each included participants with prodromal AD, mild AD dementia and mild-to-moderate AD dementia. We rated the risks of bias of all trials as low. One study (in prodromal AD) was funded by European grants. The other two studies were funded by the manufacturer of Souvenaid. One trial investigated the incidence of dementia in people with prodromal AD at baseline, and found little to no difference between the Souvenaid group and the placebo group after 24 months (RR 1.09, 95% CI 0.82 to 1.43; 1 trial, 311 participants; moderate quality of evidence). In prodromal AD, and in mild and mild-to-moderate Alzheimer's disease dementia, Souvenaid probably results in little or no difference in global or specific cognitive functions (moderate quality of evidence). Everyday function, or the ability to perform activities of daily living, were measured in mild and mild-to-moderate AD dementia. Neither study found evidence of a difference between the groups after 24 weeks of treatment (moderate quality of evidence). Two studies investigated combined cognitive-functional outcomes with the Clinical Dementia Rating Sum of Boxes and observed conflicting results. Souvenaid probably results in slight improvement, which is below estimates of meaningful change, in participants with prodromal Alzheimer's disease after 24 months (moderate quality of evidence), but probably has little to no effect in mild-to-moderate Alzheimer's disease dementia after 24 weeks (moderate quality of evidence). Adverse effects observed were low in all trials, and the available data were insufficient to determine any connection with Souvenaid. Authors' conclusions Two years of treatment with Souvenaid probably does not reduce the risk of progression to dementia in people with prodromal AD. There is no convincing evidence that Souvenaid affects other outcomes important to people with AD in the prodromal stage or mild-to-moderate stages of dementia. Conflicting evidence on combined cognitive-functional outcomes in prodromal AD and mild AD dementia warrants further investigation. Adverse effects of Souvenaid seem to be uncommon, but the evidence synthesised in this review does not permit us to make a definitive statement on the long-term tolerability of Souvenaid. The effects of Souvenaid in more severe AD dementia or in people with AD at risk of nutritional deficiencies remain unclear.

Dementia in people with intellectual disability: Insights and challenges in epidemiological research with an at-risk population

The population with intellectual disability (ID) is ageing, but age-related health concerns such as dementia have received little research attention thus far. We review evidence regarding the prevalence and incidence of dementia in people with ID, and discuss some possible explanations for an increased risk, such as shared genetic risk factors, co-morbid physical and mental disorders, lifestyle factors, trauma, and lowered brain reserve. We discuss practical and theoretical challenges facing researchers in this field, before highlighting the implications of findings to date for future research and clinical care. Research on dementia in this at-risk population has the potential to help us understand dementia in general and to improve services for this group of vulnerable individuals.