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Two functionally distinct amyloid-β intermediates link aggregation pathways to pathology in Alzheimer's disease

This study identifies two distinct amyloid-β intermediates that drive Alzheimer's pathology and shows their suppression reduces plaque burden and improves cognition in mice.

Secondary nucleation of α-Synuclein drives Mitochondria dysfunctions and Lewy body formation in Parkinson's Disease

This study identifies secondary nucleation of α-Synuclein as the key mechanism driving mitochondrial dysfunction and Lewy body formation in Parkinson's Disease.

Molecular determinants of protein pathogenicity at the single-aggregate level

This study investigates how variations in protein aggregate size, composition, and mutations affect biological functions in Alzheimer's and Parkinson's diseases.

Co-aggregation with Apolipoprotein E modulates the function of Amyloid-β in Alzheimer's disease

The paper shows that apoE isoforms modulate Aβ aggregation, clearance, and toxicity in Alzheimer's disease, with implications for therapeutic strategies.

Deficits in mitochondrial function and glucose metabolism seen in sporadic and familial Alzheimers disease derived Astrocytes are ameliorated by increasing hexokinase 1 expression.

This study shows that AD astrocytes have reduced mitochondrial and glycolytic function, which can be improved by increasing hexokinase 1 expression.

Structural conversion of α-synuclein at the mitochondria induces neuronal toxicity

The paper tracks α-synuclein conformational changes in neurons and shows mitochondrial involvement in oligomerization and toxicity.

ADSoluble aggregates present in cerebrospinal fluid change in size and mechanism of toxicity during Alzheimer's disease progression

The paper examines soluble Aβ aggregates in CSF from AD, MCI, and healthy controls, finding stage-specific differences in aggregate size and toxicity mechanisms.