Amyloid-beta
Biomarker6 papers4 findings
In mouse models, amyloid-beta levels rise under chronic restraint stress, whereas Arc-engineered exosomes and EN6-mediated mTORC1 inhibition decrease them. Additionally, BAG3 knockout impairs amyloid-beta in cultured human astrocytes.
- Animals3
- Cells2
Interventions
4EN6
downin mice1
1 study
EN6
downin mice1
EN6 decreases amyloid-beta in mice.
“Crucially, targeted mTORC1 inhibition with EN6 ameliorated autophagy-related abnormalities and was associated with reduced BACE1 abundance and CTFβ generation, together with a diminished global Aβ burden.”
AnimalsmTORC1 inhibition
Chronic stress accelerates Alzheimer pathology in mice by hyperactivating mTORC1 · CNS neuroscience & therapeutics · 29 Sep 2026
Chronic restraint stress
upin mice1
1 study
Chronic restraint stress
upin mice1
Chronic restraint stress increases amyloid-beta in mice.
“These network deficits were accompanied by accelerated AD hallmarks, including elevated Aβ deposition, dystrophic neurite aggravation, and reactive gliosis.”
Animalsin 5xFAD mice
Chronic stress accelerates Alzheimer pathology in mice by hyperactivating mTORC1 · CNS neuroscience & therapeutics · 29 Sep 2026
BAG3 knockout
downin human cells1
1 study
BAG3 knockout
downin human cells1
BAG3 knockout impairs amyloid-beta in human cells.
Cellscocultured with APP/PSEN1 mutant neuronsCRISPR/Cas9 editingastrocyte
Astrocytic BAG3 regulates protein clearance systems linked to Alzheimer disease · Proceedings of the National Academy of Sciences of the United States of America · 28 Sep 2026
Arc-engineered exosomes
downin animals1
1 study
Arc-engineered exosomes
downin animals1
Arc-engineered exosomes decrease amyloid-beta.
AnimalsAlzheimer's diseaseneural stem cell-derived exosomes overexpressing Arc
Intranasal Arc-engineered exosomes reduce Alzheimer pathology by restoring autophagy · Nanomedicine : nanotechnology, biology, and medicine · 25 Sep 2026
Latest
8Directly converted human neuronal spheroids preserve donor age and model Alzheimer disease
The three-dimensional cell platform maintains biological aging markers while spontaneously developing hallmark pathologies of sporadic Alzheimer disease.
Astrocytic BAG3 regulates protein clearance systems linked to Alzheimer disease
Loss of the chaperone mediator in human astrocytes disrupts autophagy, proteasomes, and retromer traffic while impairing amyloid-beta proteostasis in neuron cocultures.
Chronic stress accelerates Alzheimer pathology in mice by hyperactivating mTORC1
Inhibiting mTORC1 restored autophagy, reduced amyloid accumulation, and corrected circuit desynchronization and behavioral deficits in stressed Alzheimer model mice.
Activating soluble guanylate cyclase restores amyloid-beta and LDL clearance in aged rats
Cinaciguat reversed endothelial defenestration and restored paracrine signaling that enables rat hepatocytes to clear circulating lipids and amyloid-beta.
Aging rhesus macaques display distinct fluid proteomic signatures of senescence and neuropathology
Plasma proteins tracked aging and amyloid pathology more closely than cerebrospinal fluid across the non-human primate lifespan.
Intranasal Arc-engineered exosomes reduce Alzheimer pathology by restoring autophagy
The targeted nanoplatform cleared amyloid deposits and suppressed neuroinflammation in an Alzheimer's model by inhibiting mTOR signaling.