Alzheimer's disease articles from across Nature Portfolio

Staging Alzheimer’s disease on the basis of the disease’s biological underpinnings might help with stratification and prognostication, both in the clinical setting and in clinical trials. We propose a staging model based on only five biomarkers, which are related to amyloid-β and tau pathologies in different ways and can be measured with a single sample of cerebrospinal fluid.

Neuroinflammation and microglia significantly contribute to Alzheimer’s disease pathology, depending on their activation state. We found that TREM2-expressing microglia are a heterogenous population spanning activated to senescent cells.

Bueichekú et al. use multimodal in vivo neuroimaging to investigate the brain characteristics of individuals presenting unawareness of memory loss who are at risk of Alzheimer’s disease due to age. They find unawareness of memory decline is an early behavioral sign that a person might develop Alzheimer’s disease.

Two new studies show that clearance of waste, including pathogenic amyloid, through the glymphatic system is driven by synchronized neuronal activity.

Staging Alzheimer’s disease on the basis of the disease’s biological underpinnings might help with stratification and prognostication, both in the clinical setting and in clinical trials. We propose a staging model based on only five biomarkers, which are related to amyloid-β and tau pathologies in different ways and can be measured with a single sample of cerebrospinal fluid.

Levels of a host of molecules in the cerebrospinal fluid reliably assess development of the disease.

Longitudinal data from the China Cognition and Aging Study map the sequential biomarker changes that begin almost two decades before clinical onset of Alzheimer’s disease.

Epidemiological studies reveal a correlation between hearing loss and the development and progression of Alzheimer’s disease (AD), but the underlying causal mechanisms remain unclear. A study now provides experimental evidence that hearing loss can promote AD via the growth differentiation factor 1 (GDF1) pathway, which may aid in developing potential AD therapeutic strategies.

Success in a trial of low-intensity ultrasound combined with an amyloid-β antibody represents a major stride towards integrating pharmacological and nonpharmacological approaches to reduce the amyloid-β load in patients with mild Alzheimer disease. This trial also highlights the potential of therapeutic ultrasound modalities to combat neurodegenerative diseases.