TABLE 3.
Activated astrocyte marker gene expression from primary gene set, and residual and rate of change of composite global cognition: adjustment for clinical factors and neuropathology
| Model | Outcome | Covariates | Predictor | Effect of 1 unit greater composite expressionestimate (SE) P-value |
|---|---|---|---|---|
| A | Residual cognition level | Age + sex + education + post mortem interval + amyloid + neurofibrillary tangle density | Composite expression of activated astrocyte genes | −0.14 (0.05) 0.0074 |
| B | Residual cognition slope | Same as A | Composite expression of activated astrocyte genes | −0.012 (0.0039) 0.0024 |
| C | Residual cognition level | A + all neuropathologiesa | Composite expression of activated astrocyte genes | −0.11 (0.03) 0.039 |
| D | Residual cognition slope | A + all neuropathologiesa | Composite expression of activated astrocyte genes | −0.0097 (0.0039) 0.012 |
| E | Residual cognition level | A +all clinical covariatesb | Composite expression of activated astrocyte genes | −0.071 (0.03) 0.0090 |
| F | Residual cognition slope | A + all clinical covariatesb | Composite expression of activated astrocyte genes | −0.011 (0.0039) 0.00362 |
a
Amyloid level, tangle density, Lewy body pathology, macroscopic cerebral infarcts, microinfarcts, TDP-43 pathology, hippocampal sclerosis, cerebral amyloid angiopathy, cerebral atherosclerosis, and arteriolosclerosis.
b
Smoking, alcohol consumption, use of sleeping pills, body mass index, vascular disease, and vascular risk factors.
Abbreviations: SE, standard error; TDP-43, TAR DNA-binding protein 43.