Abstract
Introduction Tubercolous meningitis (TBM) is an important disease leading to morbidity, disability and mortality that primarily affects children and immune-depressed patients. Specific neuromarkers predicting outcomes, severity and inflammatory response are still lacking. In recent years an increasing number of evidences show a possible role for infective agents in developing neurodegenerative diseases. Methods We retrospectively included 13 HIV-negative patients presenting with meningeal tuberculosis. Lumbar punctures were performed for clinical reasons and CSF biomarkers were routinely available: we analyzed blood brain barrier permeability (CSF to serum albumin ratio, “CSAR”), intrathecal IgG synthesis, (CSF to serum IgG ratio), inflammation (neopterin), amyloid deposition (1-42 β-amyloid), neuronal damage (T-tau, P-tau, 14.3.3) and astrocytosis (S-100 β). Results Patients were 83% male and 67 % Caucasian with a median age of 51 years(24.5-63.5 IQR). Apart from altered CSAR (median value 18.4, 17.1-30.9 IQR), neopterin (14.3 ng/ml, 9.7-18.8) and IgG ratios (15.4, 7.9-24.9) patients showed very low levels of 1-42 β-amyloid in their CSF (348.5 pg/mL,125-532.2). Protein 14.3.3. tested altered in 38.5% cases. T-tau, ptau and S100Beta were in the range of normality. Altered low level of beta amyloid correlated over time with classical TBm findings and altered neuromarkers.Conclusion CSF Biomarkers from patients with TBM were compatible with inflammation, blood brain barrier damage and impairment in beta amyloid metabolism. Aβ1-42 could be tested as a prognostic markers, backing the routine use of available neuromarkers. To our knowledge this is the first case showing such low levels of Aβ1-42 in TBM; its accumulation, drove by neuroinflammation related to infections, can be central in understanding neurodegenerative diseases.
Low Cerebrospinal Fluid Beta Amyloid1-42 in Patients with Tubercoulous Meningitis
