This article supports SDG 3 by assessing the changes in mortality rate and years of life lost associated with dementia attributable to high BMI in China. The findings suggest a rapid increase in dementia burden attributable to high BMI.

PLCγ2 is genetically linked to Alzheimer’s disease (AD), but it is unclear how PLCγ2 contributes to pathology. Tsai et al. demonstrate that AD-associated PLCG2 variants bidirectionally orchestrate microglial responses to plaques and impact neural function in an AD mouse model. This positions PLCγ2 as a key microglial signaling node and shows that targeting PLCγ2 could have therapeutic benefits in AD.

How Phonetic-phonological impairments reflect on each stage of the Alzheimer's Disease (AD)

Training interventions with psychodrama for formal caregivers of those with dementia

This review integrates the current evidence and potential mechanisms of gut microbiota and its metabolites in Alzheimer’s disease and comprehensively reviews the possibility of leveraging dietary interventions to prevent Alzheimer’s disease progression, with a focus on the gut–microbiota–brain connections and diet–metabolite–host interactions.

In this review, we discuss how cellular senescence contributes to brain aging and neurodegenerative diseases, and the relationship between protein aggregation and cellular senescence.

This paper concludes that findings suggest that 1) long-term omega-3 fatty acid supplementation may reduce risk of Alzheimer’s disease (AD); 2) dietary omega-3 fatty acid intake, especially DHA, may lower risk of dementia or cognitive decline; and 3) peripheral biomarkers of omega-3 fatty acids may serve as predictors of cognitive decline. However, further investigation is needed to understand the gene–environment interactions involved in the intake of omega-3 fatty acids.

Alzheimer disease (AD) is a neurodegenerative condition defined by the build-up of amyloid plaques in the brain and intraneuronal tangles of the protein tau. Autophagy is a cellular cleaning process involved in the degradation of proteins, including proteins directly responsible for amyloid plaques, but its activity is compromised in AD. This study showed that reducing dietary protein intake can reduce mTORC1 activity and amyloid plaque deposition in the brains of male mice with a less aggressive model of Alzheimer's disease, but not in a more aggressive model or in female mice.

The paper proposes that Alzheimer's disease may be the consequence of a maladaptation to an evolutionary-based survival pathway triggered by fructose metabolism, which initially helps preserve critical brain functioning during starvation but becomes injurious when engaged for extensive periods. Although more studies are needed on the role of fructose metabolism and its metabolite, uric acid, in Alzheimer’s disease, it is suggested that both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be performed to determine whether there is potential benefit in the prevention, management, or treatment of this disease.

This study examined the cross-sectional and retrospective longitudinal associations between erythrocyte omege 3 (ω-3) index and cognition, brain imaging, and biomarkers among older adults. Longitudinally, low ω-3 index was associated with greater Aβ accumulation and WMS cognitive decline but unexpectedly with lower total Alzheimer’s Disease Assessment Scale cognitive subscale (ADAS-Cog) cognitive decline. Although no associations were cross-sectionally found in the whole population, low ω-3 index was associated with lower WMS cognition and higher tau accumulation among ApoE ε4 carriers.