Excerpt:

ABSTRACT: BACKGROUND: The metabolism of amyloid precursor protein
(APP) and beta-amyloid (Abeta) is widely studied in Alzheimer’s
disease, where Abeta deposition and plaque development are
essential components of the pathogenesis.
However, the physiological role of amyloid in the adult nervous
system remains largely unknown. We have previously found altered
cerebral amyloid metabolism in other neuroinflammatory
conditions. To further elucidate this, we investigated amyloid
metabolism in patients with Lyme neuroborreliosis (LNB).

METHODS: The
first part of the study was a cross-sectional cohort study in 61
patients with acute facial palsy (19 with LNB and 42 with
idiopathic facial paresis, Bell’s
palsy) and 22 healthy controls. CSF was analysed for the
beta-amyloid peptides Abeta38, Abeta40 and Abeta42, and the
amyloid precursor protein (APP) isoforms alpha-sAPP and
beta-sAPP. CSF total-tau (T-tau), phosphorylated tau (P-tau) and
neurofilament protein (NFL) were measured to monitor neural cell
damage. The second part of the study was a prospective
cohort-study in 26 LNB patients undergoing consecutive lumbar
punctures before and after antibiotic treatment to study
time-dependent dynamics of the biomarkers.

RESULTS: In the cross-sectional
study, LNB patients had lower levels of CSF alpha-sAPP, beta-sAPP
and P-tau, and higher levels of CSF NFL than healthy controls and
patients with Bell’s palsy.
In the prospective study, LNB patients had low levels of CSF
alpha-sAPP, beta-sAPP and P-tau at baseline, which all increased
towards normal at follow-up.