Table 2 Summary of preclinical studies on patients with sporadic AD

55

4

73

8

CSF T-tau was cross-sectionally correlated with MMSE score. CSF Aβ42 was correlated with future MMSE and change in MMSE.

There were only women in this study.

[16]

61

13 (had a CDR > 0)

75

3-4

No significant results for Aβ42, T-tau, P-tau in CSF.

The main outcome was to predict conversion from CDR 0 to a higher CDR. The CSF T-tau:Aβ42 and P-tau:Aβ42 ratios significantly predicted this.

[17]

51

0

73

3

↓ Aβ42 in CSF predicted cognitive decline. No significant results for T-tau or P-tau in CSF.

Cognition was evaluated with memQoL and MMSE. The combination of CSF Aβ42 and P-tau predicted cognitive decline with increased accuracy compared with Aβ42 alone.

[18]

37

0

73

4.5

↓ Aβ42 CSF at follow-up correlated with worse cognition. Individuals with the most substantial longitudinal decrease of Aβ42 or increase of P-tau in CSF performed worse on cognitive test than the others. No significant results for CSF T-tau and plasma Aβ42.

Cognition was evaluated with ADAS-cog and AQT.

[19]

43

0, but 4 developed MCI

Around 69^a

3.5

Aβ42 and T-tau in CSF were used for predicting MCI.

Individuals were dichotomized into having a high or normal CSF T-tau/Aβ42 ratio. Individuals with a high ratio were more likely to develop MCI on follow-up.

[20]

35

7

85

3

↓Aβ42 in CSF at baseline in patients that developed dementia. The CSF Aβ42:Aβ40 ratio showed a tendency to be lower (p = 0.068) in individuals that developed dementia.

CSF Aβ40 was lower in patients with dementia at baseline, but could not predict dementia in the cognitively normal.

[21]

127

2, and 11 developed MCI

60

4

↓Aβ42, ↑T-tau and ↑ P-tau in CSF among progressors.

All patients had subjective complaints at baseline. CSF Aβ42 alone was the strongest predictor for clinical progression.

[22]