Abstract Body: Collateral development plays an important role in maintaining cerebral blood flow (CBF) in the presence of critical stenosis or occlusion of large cerebral arteries. Age is a non-modifiable risk factor for ischemic stroke associated with collateral rarefaction. Here, we studied the influence of aging on collateral development and cerebral hemodynamic impairment using 114 mice (56 male and 58 female, C57/BL6) of two age groups (young: 20 ± 2 weeks; aged: 71 ± 9 weeks). We permanently occluded the right common carotid artery (RCCAO) via suture ligation and compared these to sham-operated animals. We quantified the diameters of major branches of the circle of Willis and pial collaterals using black ink angiograms 4 weeks after the procedure. In a separate cohort, CBF was measured in the dorsal cortex using laser speckle imaging 3 hours (acute) and 4 weeks (chronic) after RCCAO or sham. Regions of interest were placed on both hemispheres in the major arterial territories and watersheds. To evaluate cerebrovascular reserve, we induced hypotension by controlled exsanguination. In young mice, compared with sham, RCCAO led to a significant increase in the diameters of the right anterior cerebral artery (ACA), the left anterior cerebral artery (ACA), and the right posterior communicating artery (PCommA), suggesting collateral growth (increase rate 30%, 27%, and 66%, respectively). The diameters of pial collaterals were also increased bilaterally. In aged mice, the circle of Willis and pial collateral growth were both diminished after RCCAO compared with sham (increase rate 14% right ACA, 19% left ACA, and 10% right PCommA). Laser speckle imaging revealed a reduction in CBF upon acute RCCAO in both age groups, which was slightly worse in aged mice. In young mice, baseline CBF recovered completely 4 weeks after RCCAO, but cerebrovascular reserve appeared mildly reduced during hypotension. In aged mice, recovery of baseline CBF was incomplete in all vascular territories, and cerebrovascular reserve appeared markedly diminished during hypotension. In conclusion, our study reveals that aging causes diminished collateral growth potential, which is a strong determinant of hemodynamic impairment at baseline and cerebrovascular reserve during hypotension. The molecular underpinnings of this collateral deficit remain to be elucidated.