The cerebrospinal fluid (CSF)
biomarker profile in
Alzheimer's disease (AD) is characterized by decreased
beta amyloid (Aβ(1-42)), increased total and hyperphosphorylated tau (t-tau and p-tau, respectively), which is a useful diagnostic tool and gives insight in the pathogenesis of AD. It is of importance to study how these
biomarkers react in other
CNS diseases; therefore, we decided to analyse
amyloid and tau
biomarkers in different
CNS infections. We also included analysis of soluble
amyloid precursor
proteins (sAPPα and -β). CSF Aβ(1-42), sAPPα and -β, t-tau and p-tau were analysed in
bacterial meningitis (n = 12),
Lyme neuroborreliosis (n = 13), herpes simplex virus type 1 (HSV-1)
encephalitis (n = 10), HIV-associated
dementia (HAD) (n = 21), AD (n = 21) and healthy controls (n = 42). Concurrent with AD, Aβ(1-42) was decreased in all groups except neuroborreliosis compared to controls. HSV-1
encephalitis,
bacterial meningitis and HAD showed lower concentrations of sAPPα and -β compared to AD. T-tau was increased in AD and HSV-1
encephalitis compared to all other groups. P-tau was higher in AD and HSV-1
encephalitis compared to
bacterial meningitis, HAD and control. Decreased CSF Aβ(1-42), sAPPα and -β in various
CNS infections imply an effect of
neuroinflammation on
amyloid metabolism which is similar in regard to AD concerning Aβ(1-42), but differs concerning sAPPα and -β. These results clearly indicate different pathologic pathways in AD and infectious
CNS disease and may provide help in the differential
biomarker diagnostics. Increased p-tau in HSV-1
encephalitis probably reflect acute neuronal damage and
necrosis.