Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis

Abstract Background Tuberculous 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 i...

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Autores principales:	Giacomo Stroffolini, Giulia Guastamacchia, Sabrina Audagnotto, Cristiana Atzori, Mattia Trunfio, Marco Nigra, Alessandro Di Stefano, Giovanni Di Perri, Andrea Calcagno
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Tuberculosis Meningitis Alzheimer’s disease Amyloid-beta Neuromarkers Dementia Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/970cbc7e4b054fb992e06f008cb426ae
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spelling	oai:doaj.org-article:970cbc7e4b054fb992e06f008cb426ae2021-11-21T12:09:37ZLow cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis10.1186/s12883-021-02468-21471-2377https://doaj.org/article/970cbc7e4b054fb992e06f008cb426ae2021-11-01T00:00:00Zhttps://doi.org/10.1186/s12883-021-02468-2https://doaj.org/toc/1471-2377Abstract Background Tuberculous 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 TBM and we compared them with two control groups: one of patients with a confirmed diagnosis of AD, and one of those with syphilis where lumbar punctures excluded central nervous system involvement. 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 (Aβ1–42), neuronal damage (T-tau, P-tau, 14.3.3) and astrocytosis (S-100 β). Results TBM 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 Aβ1–42 in their CSF (348.5 pg/mL,125-532.2), even lower compared to AD and controls [603 pg/mL (IQR 528–797) and 978 (IQR 789–1178)]. Protein 14.3.3 tested altered in 38.5 % cases. T-tau, P-tau and S100Beta were in the range of normality. Altered low level of Aβ1–42 correlated over time with classical TBM findings and altered neuromarkers. Conclusions CSF Biomarkers from patients with TBM were compatible with inflammation, blood brain barrier damage and impairment in amyloid-beta metabolism. Amyloid-beta 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.Giacomo StroffoliniGiulia GuastamacchiaSabrina AudagnottoCristiana AtzoriMattia TrunfioMarco NigraAlessandro Di StefanoGiovanni Di PerriAndrea CalcagnoBMCarticleTuberculosisMeningitisAlzheimer’s diseaseAmyloid-betaNeuromarkersDementiaNeurology. Diseases of the nervous systemRC346-429ENBMC Neurology, Vol 21, Iss 1, Pp 1-8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Tuberculosis Meningitis Alzheimer’s disease Amyloid-beta Neuromarkers Dementia Neurology. Diseases of the nervous system RC346-429
spellingShingle	Tuberculosis Meningitis Alzheimer’s disease Amyloid-beta Neuromarkers Dementia Neurology. Diseases of the nervous system RC346-429 Giacomo Stroffolini Giulia Guastamacchia Sabrina Audagnotto Cristiana Atzori Mattia Trunfio Marco Nigra Alessandro Di Stefano Giovanni Di Perri Andrea Calcagno Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
description	Abstract Background Tuberculous 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 TBM and we compared them with two control groups: one of patients with a confirmed diagnosis of AD, and one of those with syphilis where lumbar punctures excluded central nervous system involvement. 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 (Aβ1–42), neuronal damage (T-tau, P-tau, 14.3.3) and astrocytosis (S-100 β). Results TBM 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 Aβ1–42 in their CSF (348.5 pg/mL,125-532.2), even lower compared to AD and controls [603 pg/mL (IQR 528–797) and 978 (IQR 789–1178)]. Protein 14.3.3 tested altered in 38.5 % cases. T-tau, P-tau and S100Beta were in the range of normality. Altered low level of Aβ1–42 correlated over time with classical TBM findings and altered neuromarkers. Conclusions CSF Biomarkers from patients with TBM were compatible with inflammation, blood brain barrier damage and impairment in amyloid-beta metabolism. Amyloid-beta 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.
format	article
author	Giacomo Stroffolini Giulia Guastamacchia Sabrina Audagnotto Cristiana Atzori Mattia Trunfio Marco Nigra Alessandro Di Stefano Giovanni Di Perri Andrea Calcagno
author_facet	Giacomo Stroffolini Giulia Guastamacchia Sabrina Audagnotto Cristiana Atzori Mattia Trunfio Marco Nigra Alessandro Di Stefano Giovanni Di Perri Andrea Calcagno
author_sort	Giacomo Stroffolini
title	Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
title_short	Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
title_full	Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
title_fullStr	Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
title_full_unstemmed	Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis
title_sort	low cerebrospinal fluid amyloid-βeta 1–42 in patients with tuberculous meningitis
publisher	BMC
publishDate	2021
url	https://doaj.org/article/970cbc7e4b054fb992e06f008cb426ae
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Low cerebrospinal fluid Amyloid-βeta 1–42 in patients with tuberculous meningitis

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