Beyond amyloid: Contributions of neuroinflammation, cerebrovascular disease, and neurodegeneration to memory impairment in the oldest‐old, the LifeAfter90 Study

Parallel neuroinflammatory pathways to cerebrovascular burden and amyloid beta in Alzheimer's disease

Higher plasma YKL‐40 was associated with greater white matter hyperintensity (WMH), whereas higher plasma GFAP was related to increased 18F‐florbetapir (FBP) standardized uptake value ratio (SUVR) and higher plasma p‐tau217 was associated with reduced MTL cortical thickness and hippocampal volume.

Post mortem MRI of cholinergic white matter pathways across neurodegenerative diseases

Cholinergic white matter pathway degeneration is central in Alzheimer's disease and Lewy body disease and can be assessed in vivo using magnetic resonance imaging proxies, but neuropathological validation is limited.

Soluble pathogenic tau transmission to astrocytes drives acute oxidative damage, cellular senescence, and neurovascular uncoupling in a model of Alzheimer’s tauopathy

Changes in serum β‐synuclein precede blood biomarkers of Alzheimer pathology in Down syndrome

There is a need for early, objective markers of Alzheimer's disease (AD)‐related synapse dysfunction in adults with Down syndrome (DS). The presynaptic protein β‐synuclein is elevated in the blood of adults with DS. This study evaluates the positioning of these changes relative to changes in pathophysiological blood bi...

Applying a systemic approach that extends beyond the brain to Alzheimer’s disease pathogenesis

Traditional dementia research often isolates single aspects, biomarkers or symptoms, overlooking complex interactions shaping disease risk and progression. Lysosomal and mitochondrial dysfunction, reflecting systemic processes, may explain links between Alzheimer’s and metabolic, inflammatory, cardiovascular, ageing, g...

APOE4 astrocytes call the shots on neuronal α-synuclein pathology.

The results suggest that APOE4 increases cholesterol levels and impairs lysosomal function in astrocytes, which release pathogenic α-Syn inclusions in APOE4 carriers.