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Low plasma neurofilament light levels associated with raised cortical microglial activation suggest inflammation acts to protect prodromal Alzheimer's disease

Artikel i vetenskaplig tidskrift
Författare P. Parbo
L. S. Madsen
R. Ismail
Henrik Zetterberg
Kaj Blennow
S. F. Eskildsen
T. Vorup-Jensen
D. J. Brooks
Publicerad i Alzheimers Research & Therapy
Volym 12
Nummer/häfte 1
Sidor 7
Publiceringsår 2020
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för psykiatri och neurokemi
Sidor 7
Språk en
Länkar dx.doi.org/10.1186/s13195-019-0574-...
Ämnesord Neurofilament light, Microglia, Inflammation, PET, PK11195, MCI, Alzheimer, mild cognitive impairment, cerebrospinal-fluid, Neurosciences & Neurology
Ämneskategorier Neurovetenskaper

Sammanfattning

Background Plasma and cerebrospinal fluid levels of neurofilament light (NfL), a marker of axonal degeneration, have previously been reported to be raised in patients with clinically diagnosed Alzheimer's disease (AD). Activated microglia, an intrinsic inflammatory response to brain lesions, are also known to be present in a majority of Alzheimer or mild cognitive impaired (MCI) subjects with raised beta-amyloid load on their positron emission tomography (PET) imaging. It is now considered that the earliest phase of inflammation may be protective to the brain, removing amyloid plaques and remodelling synapses. Our aim was to determine whether the cortical inflammation/microglial activation load, measured with the translocator protein marker C-11-PK11195 PET, was correlated with plasma NfL levels in prodromal and early Alzheimer subjects. Methods Twenty-seven MCI or early AD cases with raised cortical beta-amyloid load had C-11-(R)-PK11195 PET, structural and diffusion magnetic resonance imaging, and levels of their plasma NfL measured. Correlation analyses were performed using surface-based cortical statistics. Results Statistical maps localised areas in MCI cases where levels of brain inflammation correlated inversely with plasma NfL levels. These areas were localised in the frontal, parietal, precuneus, occipital, and sensorimotor cortices. Brain inflammation correlated negatively with mean diffusivity (MD) of water with regions overlapping. Conclusion We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD. This is supported by the finding of an inverse association between cortical water diffusivity and microglial activation in the same regions. Our findings suggest a rationale for stimulating microglial activity in early and prodromal Alzheimer cases-possibly using immunotherapy. Plasma NfL levels could be used as a measure of the protective efficacy of immune stimulation and for monitoring efficacy of putative neuroprotective agents.

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