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Background and purpose  At high altitude the brain is exposed to hypoxic stress, which may result in neurological conditions, with acute mountain sickness (AMS) being the most common. We aimed to test the hypothesis that rapid ascent to high altitude alters neuro‐axonal integrity, which can be detected by increased concentration of serum neurofilament light (sNfL) in the blood and may even be exaggerated in people with AMS.    Methods  Serum neurofilament light was measured using a single‐molecule array (Simoa, Quanterix, Lexington, MA, USA) assay at low altitude (423 m) in 47 healthy study participants and 44 h after rapid and active ascent to high altitude (4559 m). Peripheral oxygen saturation (SpO 2 ) and partial pressures of oxygen (pO 2 ) were obtained at low and high altitude. The Acute Mountain Sickness‐Cerebral (AMS‐C) scoring system was used to assess AMS incidence and AMS severity.    Results  There was an increase in sNfL from its baseline value compared with its value at high altitude (6.34 ± 1.96 vs. 7.19 ± 3.14 pg/ml;  p  = 0.014), but sNfL level did not correlate with SpO 2  ( r  = −0.19;  p  = 0.066) or pO 2  ( r  = −0.19;  p  = 0.068). The incidence of AMS at high altitude was 62%. Neither at low altitude ( p  = 0.706) nor at high altitude ( p  = 0.985) was there a difference in sNfL between participants with and without AMS as measured 3 days after rapid ascent and 44 h of high‐altitude exposure. Altitude sNfL did not correlate with AMS‐C, either overall or with single‐item scores such as headache severity.    Conclusions  Rapid ascent of healthy people to high altitude provokes an increase in sNfL 44 h after arrival at 4559 m, which is not related to the magnitude of hypoxemia or AMS incidence and severity, suggesting that neuro‐axonal injury does not directly contribute to AMS.

Serum neurofilament level increases after ascent to 4559 m but is not related to acute mountain sickness