Table 1.

Studies conducted to evaluate the role of apoE as a potential CSF biomarker

Study	Study groups	CSF levels in AD/study groups	Association with APOE genotype/core markers	Analysis method
Van Harten et al. [71]	Non-demented individuals (n = 430) classified into subjective cognitive decline (SCD, n = 207) or mild cognitive impairment (MCI, n = 213)	CSF levels were higher in MCI compared to SCD at baseline, on stratification of MCI and SCD into ε4 and non-ε4 carriers and significant difference was seen only in ε4 carriers	CSF levels were strongly associated with CSF T-tau and P-tau in APOE ε4 carriers	ELISA
Johansson et al. [72]	AD (n  = 29), other dementias (n  =  4), stable cognitive function (SMCI, n  = 13) and healthy controls (n = 18)	CSF levels were significantly elevated in AD compared to other dementia and lower as compared to healthy controls	ApoE levels in CSF were not associated with APOE genotype	Luminex multiplex assay
Rezeli et al. [73]	AD (n = 13) and non-AD (n = 12)	No significant difference between study groups	ApoE levels in CSF were not associated with APOE genotype; CSF levels positively correlated with P-tau in ε4 non-carriers	Mass spectrometry
Richens et al. [74]	AD (n = 10) and controls (n = 18)	No significant difference between study groups		Luminex multiplex assay
Toledo et al. [75]	Normal controls (n = 92), MCI (n = 149) and AD (n = 69)	CSF apoE levels were associated with cognitive decline and atrophy rate	Results were only significant in the group without the ε4 allele	Luminex multiplex assay
Perrin et al. [76]	Cognitively normal [clinical dementia rating (CDR 0, n = 24) and mild AD or probable AD (CDR 1, n = 24)]	Did not differ significantly between the two groups		ELISA
Zhang et al. [61]	AD (n = 48), Parkinson’s disease (PD, n = 40), controls (n = 95)	Reduced in AD as compared to controls, but did not differ from PD		Multiplex assay
Hesse et al. [68]	AD patients (n = 55) and normal controls (n = 21)	Reduced in AD as compared to the controls	Individuals having ε4 allele had higher apoE levels	ELISA
Fukuyama et al. [66]	AD patients, n = 25 [early onset Alzheimer’s disease (EOAD) and late onset Alzheimer’s disease (LOAD)] and normal controls (n = 36)	ApoE levels were reduced with age in normal controls and increased in AD (more distinctly in EOAD). The elevated levels were positively correlated with decline in cognition		ELISA
Pirttilä et al. [64]	AD (n = 25); classified as APOE ε4 positive (n = 16) and negatives (n = 9), and as mild (n = 16) and moderate dementia (n = 9)	ApoE levels decreased with time in ε4 positives and in both mild and moderate dementia		ELISA
Lindh et al. [65]	AD (n = 18), MCI (n = 9), other dementia disorders (ODD, n = 9) and age-matched healthy controls	Elevated in AD, MCI and ODD as compared to healthy controls and significantly increased in AD at follow-up	CSF levels significantly correlated with CSF tau in AD	ELISA
Merched et al. [67]	AD (n = 38), controls (n = 31) and those suffering from other neurological disorders (n = 47)	Significantly elevated in patients with LOAD as compared to controls and other neurological disorders		ELISA
Landen et al. [63]	EOAD (n = 23), LOAD (n = 31), frontotemporal dementia (FTD, n = 16), vascular dementia (VaD, n = 25) and controls (n = 25)	Significantly reduced in all the groups compared to the controls, in EOAD compared to LOAD and FTD	ApoE levels in CSF were not influenced by APOE genotype	ELISA
Blennow et al. [62]	AD (n = 11), FTD (n = 10) and controls (n = 10)	Significantly reduced in AD as compared to the controls and FTD group. Also, significantly reduced in FTD as compared to controls		ELISA