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. 2024 Jan 27;25(3):1584. doi: 10.3390/ijms25031584

Table 1.

Proteins altered in bdEP may constitute putative biomarker candidates for AD. Protein signal abundance detected in the microarray analysis of bdEP isolated from Controls and AD cases. Their role and alteration pattern in AD brain are summarized.

Gene Name UniProt ID Antibody P-Site C Mean AD Mean %CFC p-Value Relevance in AD Levels in AD Brain Ref
MFN2 O95140 Pan 2410 1032 −57 0.009 MFN2 down-regulation impairs γ-secretase activity and decreases Aβ production;
Decreased mRNA and protein levels in the brains of AD patients and AD transgenic mice
↓ mRNA and protein in humans or mice [43,44,45,46]
ATF2 P15336 Pan 317 141 −56 0.020 MAPK signaling, induced by Aβ, activates ATF2, resulting in an inflammatory response by astrocytes ↓/↑
In humans
[47,48,49,50,51,52]
NTRK2 Q16620 Y706 + Y707 1708 2247 32 0.039 Risk gene in AD: Binds and phosphorylates APP at Y687, retaining APP in TGN, and decreasing Aβ production ↓ pan in humans and mice [58,59,60]
PRKAA1 Q13131 T183 + S184 4926 6566 33 0.039 Tau kinase, co-localized with neurofibrillary tangles ↑ pan in human [55,56]
TAOK1 * Q7L7 × 3 S181 262 419 60 0.023 Tau kinase, active and co-localized with neurofibrillary tangles ↑ active (S181) human [53]
GRK1 Q15835 Pan 288 615 114 0.017 Unknown - -

* For TAOK1, distinct phosphorylated residues were found to be either increased or decreased. Abbreviations: AD, Alzheimer’s disease; C, Controls; CFC, Percentage of change from Controls; TGN, Trans-Gogi network; ↓ decreased; ↑ increased.