Skip to main content
. 2017 Feb 15;37(7):1675–1684. doi: 10.1523/JNEUROSCI.3047-16.2016

Table 4.

Multiple regression analyses

β t test p
CVLT Trials 1–5
    CA1 α-synuclein −0.237 −2.40 0.019
    CA1 plaques −0.054 −0.49 0.620
    CA1 tangles −0.395 −3.35 0.001
    Test–death interval 0.537 4.97 0.000
CVLT short delay
    CA1 α-synuclein −0.255 −2.47 0.016
    CA1 plaques 0.047 0.42 0.679
    CA1 tangles −0.472 −3.84 0.000
    Test–death interval 0.409 3.63 0.001
CVLT long delay
    CA1 α-synuclein −0.203 −1.96 0.053
    CA1 plaques 0.067 0.59 0.559
    CA1 tangles −0.498 −4.03 0.000
    Test–death interval 0.422 3.73 0.000
CVLT recognition
    CA1 α-synuclein −0.131 −1.16 0.251
    CA1 plaques −0.009 −0.07 0.941
    CA1 tangles −0.335 −2.47 0.016
    Test–death interval 0.279 2.25 0.028
Visual reproduction: immediate
    CA1 α-synuclein −0.258 −2.36 0.021
    CA1 plaques 0.159 1.32 0.193
    CA1 tangles −0.395 −2.93 0.005
    Test–death interval 0.476 3.86 0.000
Visual reproduction: delay
    CA1 α-synuclein −0.304 −2.81 0.006
    CA1 plaques 0.105 0.88 0.383
    CA1 tangles −0.481 −3.62 0.001
    Test–death interval 0.380 3.13 0.003

The degree of α-synuclein pathology in CA1 of the hippocampus makes a significant independent contribution to the memory deficit of patients with DLB, above and beyond the significant contribution made by the burden of CA1 AD tangle pathology. The same pattern of results was observed for the CVLT Trial 1–5 learning measure when total hippocampal α-synuclein burden (rather than just CA1) was used in the first model. All models were highly significant (p values < 0.001). Standardized β values and significance levels for inclusion in the various models are shown for each variable.