Intrathecal chemokine levels in Alzheimer disease and frontotemporal lobar degeneration

Amyloid beta (Aβ)1–42 deposition into the brain is considered a crucial pathogenetic step during Alzheimer disease (AD) development, as it originates a cascade of events leading to irreversible neuronal damage.1 Conversely, frontotemporal lobar degeneration (FTLD) is characterized by intracellular deposition of abnormally phosphorylated tau protein responsible for neuronal death.2 Immunoreactivity for a number of chemokines and for their related receptors has been demonstrated in resident cells of the CNS.3 Some of them have been proposed as candidate genes for AD,4 and increased levels have been found in CSF from patients with AD,5 whereas no information on chemokines in FTLD is available at present. Interferon-γ-inducible protein-10 (IP-10), monocyte chemotactic protein-1 (MCP-1), and interleukin-8 (IL-8) levels were evaluated in CSF from 32 patients with probable AD (11 men and 21 women; mean age at onset: 62.1 ± 8.0 years), 24 with FTLD (frontotemporal dementia [FTD] = 17; progressive aphasia [PA] = 5; semantic dementia [SD] = 2; 9 men and 15 women; mean age at onset: 61.5 ± 1.6 years). …