Data and code from: Hemodynamic and neuronal contributions to low-frequency vascular oscillations in a preclinical model of Alzheimer's disease

Significance: Vasomotion, a temporal oscillation in vascular diameter
centered around 0.1 Hz, may be altered in Alzheimer’s disease (AD), with
both increases and decreases reported.  Aim: The current study
aimed to better characterise vasomotion in vivo, assess its feasibility as
an early biomarker for vascular dysfunction in AD, and determine the
relationship of vasomotion to underlying neuronal activity. Approach:
Low-frequency (0.06 - 0.2 Hz) oscillations (LFOs) in the cerebral arteries
of anaesthetised 9-12 month-old J20-AD (n = 12) and wild-type (n = 10)
mice were extrapolated from haemodynamic data obtained using 2-dimensional
optical imaging spectroscopy (2D-OIS). Changes in LFO power were
determined after an inspired gas challenge and compared between groups.
Simultaneously gathered multi-unit neuronal activity data were used to
determine whether LFOs were independent of neural activity. 
Results: LFOs increased as inspired oxygen was reduced, but the change in
LFO power did not differ between groups. LFOs were found to be driven by
neuronal activity, suggesting that they represent spontaneous
low-frequency neurovascular coupling rather than vascular-only derived
activity. Conclusions: Arterial LFOs obtained by 2D-OIS were not a
suitable metric to distinguish anaesthetised J20-AD males from healthy
male controls. Further, haemodynamic oscillations occurring within the
same frequency range as vasomotion may reflect underlying neuronal
activity.