Back

Early Alzheimer's disease pathology in human cortex is associated with a transient phase of distinct cell states

Gazestani, V. H.; Kamath, T.; Nadaf, N. M.; Burris, S.; Rooney, B.; Junkkari, A.; Vanderburg, C.; Rauramaa, T.; Therrien, M.; Tegtmeyer, M.; Herukka, S.-K.; Abdulraouf, A.; Marsh, S.; Malm, T.; Hiltunen, M.; Nehme, R.; Stevens, B.; Leinonen, V.; Macosko, E. Z.

2023-06-05 genomics
10.1101/2023.06.03.543569 bioRxiv
Show abstract

Cellular perturbations underlying Alzheimers disease are primarily studied in human postmortem samples and model organisms. Here we generated a single-nucleus atlas from a rare cohort of cortical biopsies from living individuals with varying degrees of Alzheimers disease pathology. We next performed a systematic cross-disease and cross-species integrative analysis to identify a set of cell states that are specific to early AD pathology. These changes-which we refer to as the Early Cortical Amyloid Response--were prominent in neurons, wherein we identified a transient state of hyperactivity preceding loss of excitatory neurons, which correlated with the selective loss of layer 1 inhibitory neurons. Microglia overexpressing neuroinflammatory-related processes also expanded as AD pathological burden increased. Lastly, both oligodendrocytes and pyramidal neurons upregulated genes associated with amyloid beta production and processing during this early hyperactive phase. Our integrative analysis provides an organizing framework for targeting circuit dysfunction, neuroinflammation, and amyloid production early in AD pathogenesis.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.