Impaired brain glucose consumption is a possible trigger of Alzheimer’s disease (AD). Animal models can help characterize each contributor to the cascade independently. Here we perform a first-time longitudinal study of brain connectivity in the intracerebroventricular-streptozotocin rat model of AD. We report altered brain circuitry as early as two weeks in regions notoriously affected by AD (cingulate cortices, posterior parietal cortex and hippocampus), and widespread gradual breakdown of connectivity with time. The changes in brain connectivity induced by glucose metabolism disruption can bring further insight into the role of this mechanism in AD.