Amyloid beta (amyloid beta) is a pathogenic peptide and major protein component of amyloid plaques in alzheimers disease, where its accumulation is a hallmark of disease pathology and cerebral amyloidosis. Its generation is linked to bace1, and plasma Aβ levels are also used as a biomarker outcome in the ALPS study, reflecting its role in tracking Alzheimer’s pathophysiology. Beyond plaque formation, recent work links Aβ species to mitochondrial damage and impaired mitochondrial clearance via tomm20, and to broader pathogenic cascades alongside tau. Therapeutic and engineering efforts are focused on suppressing Aβ aggregation or enhancing its clearance, including rutin, ngn cds, rb lcp ar, and engineered nanobody formats for targeted delivery. Recent literature also highlights anti-inflammatory neuroenhancers that reduce both Aβ production and aggregation, as well as studies on post-translational modifications and mitophagy/ferroptosis pathways that may modulate Aβ-driven neurodegeneration. Overall, Aβ remains a central biomarker and therapeutic target in Alzheimer’s disease, with current advances emphasizing aggregation blockade, disaggregation of preformed fibrils, and pathway-level intervention.
Alzheimer’s disease
- Aβ accumulation was described as a hallmark of alzheimers disease, and its generation was linked to bace1-dependent processing. (PMID:41838033)
- Aβ was identified as a pathological plaque component and a major pathogenic protein alongside tau in Alzheimer’s disease. (PMID:41823685) (PMID:41944134)
- Plasma Aβ levels were measured as an outcome in the ALPS randomized trial aimed at improving cognition and Alzheimer’s pathophysiology through slow-wave sleep. (PMID:41715219)
- A 2026 Neurobiology of Aging study reported that pathogenic Aβ species accumulated consistently and were associated with mitochondrial damage and impaired mitochondrial clearance in human and rodent models. (PMID:41637762)
Therapeutic targeting and aggregation control
- rutin was reported to suppress Aβ aggregation. (PMID:41823685)
- ngn cds were described as suppressing Aβ aggregation and disaggregating preformed fibrils. (PMID:42003377)
- rb lcp ar was reported to concurrently target Aβ aggregation as part of a multi-pronged anti-Alzheimer strategy. (PMID:42003377)
- Engineered nanobody formats were highlighted as enabling specific targeting of Aβ for drug delivery systems. (PMID:41568664)
- An anti-inflammatory neuroenhancer reduced Aβ pathology, including aggregation and production, in an Alzheimer’s disease therapy context. (PMID:41696149)