Journal of Dementia and Alzheimer's Disease

Background/Objective: To examine whether patients with late-onset schizophrenia (LOS) and very-late-onset schizophrenia-like psychosis (VLOS) are at a higher risk of developing dementia than patients with early-onset schizophrenia (EOS). Methods: A random sample of incident cases of patients with schizophrenia with an age of onset after age 40 (LOS) and age 60 (VLOS) was selected from a psychiatric case register covering all psychiatric services within the city of The Hague, The Netherlands, between 1997 and 2012. Schizophrenia diagnosis and age of onset were audited by systematic review of all case notes up to 2019. Patients who were initially misclassified as LOS/VLOS in the registry but, after this audit, had an age of onset before age 40, were classified as EOS. The risk of developing dementia was compared between the groups using a logistic regression model with correction for age, gender, and stroke as possible confounders. Results: Our study groups consisted of 74 patients with EOS, 81 with LOS, and 25 with VLOS. Dementia was present in 10 patients at follow-up, 7 out of 106 (6.6%) patients in the combined LOS and VLOS groups, and 3 out of 74 (4.1%) patients in the EOS group. However, after correction for confounders, logistic regression showed no statistically significant higher change in the development of dementia in LOS nor VLOS patients compared to EOS patients, nor with age of onset as a continuous variable. Conclusions: Patients with LOS and VLOS are not at a higher risk of developing dementia compared to patients with EOS. These results do not support the hypothesis that LOS and especially VLOS, are precursors of dementia.

Background: International policy increasingly recognises the importance of inclusive, community-based support for people living with dementia. Football, as a culturally significant sport, has the potential to reach older adults and communities disproportionately affected by health inequalities. The objectives of this review were to collate evidence on football-based dementia initiatives, including intervention format, delivery approaches, and reported outcomes. Methods: Seven databases (Sportdiscus, MEDLINE, Embase, Scopus, PsycINFO, CINAHL, and Web of Science) were searched for relevant peer-reviewed and grey literature from their inception to June 2025. The PICO framework was used to define eligibility criteria. Eligible studies described community-based football-themed or football-based programmes involving people living with dementia. Data were extracted on participant sample, intervention characteristics, and reported outcomes, and iteratively charted. Results: In total, 11 of the 1059 identified articles were included within this review. Initiatives were often delivered through professional football clubs and charitable foundations, with formats ranging from reminiscence therapy sessions to walking football. Common outcomes for participants included increased sociability, improved mood, enhanced communication, and a strengthened sense of identity and belonging. Some interventions also reported physical benefits, such as improved mobility. Carers highlighted respite opportunities, peer support, and enjoyment from seeing relatives more engaged. Despite positive reports, outcome measurement was inconsistent, and most studies were small-scale or descriptive pilot projects. Conclusions: Football-based dementia initiatives provide meaningful, culturally grounded opportunities for social inclusion and support. Their delivery through community clubs/organisations positions them well to address inequities in dementia care, particularly in areas of disadvantage. However, stronger evaluation methods are required to build a robust evidence base and guide sustainable implementation at scale.

Type 2 Diabetes Mellitus (T2DM) is a recognized risk factor for Alzheimer’s Disease (AD), as epidemiological research indicates that those with T2DM have a markedly increased risk of experiencing cognitive decline and dementia. Chronic hyperglycemia and insulin resistance in T2DM hinder cerebral glucose metabolism, reducing the primary energy source for neurons and compromising synaptic function. Insulin resistance impairs signaling pathways crucial for neuronal survival and plasticity, while high insulin levels compete with amyloid-β (Aβ) for breakdown by insulin-degrading enzyme, promoting Aβ buildup. Additionally, vascular issues linked to T2DM impair blood–brain barrier functionality, decrease cerebral blood flow, and worsen neuroinflammation. Elevated oxidative stress and advanced glycation end-products (AGEs) in diabetes exacerbate tau hyperphosphorylation and mitochondrial dysfunction, worsening neurodegeneration. Collectively, these processes create a robust biological connection between T2DM and AD, emphasizing the significance of metabolic regulation as a possible treatment approach for preventing or reducing cognitive decline. Here, we review the relationship between T2DM and AD and discuss the roles insulin, hyperglycemia, and inflammation therapeutic strategies have in successful development of AD therapies. Additionally evaluated are recent therapeutic advances, especially involving the polyflavonoid anthocyanin, against T2DM-mediated AD pathology.