Objective: Alzheimer’s disease (AD) is characterized by severe cognitive deficits involving different cognitive domains such as memory decline, language deficits, and apraxia. Mild cognitive impairment (MCI) is supposed to represent a potential preclinical stage of the disease where distinct cognitive deficits occur. Although, memory impairment has been addressed in recent neuroimaging studies the neural substrates of most cognitive deficits in AD, which can be reliable be assessed by using the neuropsychological test battery of the Consortium to Establish a Register for Alzheimer’s Disease (CERAD), remain unresolved. To this concern, positron emission tomography (PET) has been proofed an adequate method for unrevealing the neural substrates of cognitive dysfunctions. Method: Seventy-five patients with AD and MCI were investigated with 18F-2-fluoro-2-deoxy-d-glucose (FDG) PET. In all patients, the neuropsychological test battery of the CERAD was applied. Using statistical parametric mapping significant correlations were calculated to assess the association of cerebral glucose metabolism and neuropsychological test performance. Results: Significant correlations between memory test scores and activation of temporo-frontal and cingulate cortices occurred. Verbal fluency and naming scores were significantly correlated with predominantly left temporo-parietal and frontal cortices whereas constructional praxis test scores were significantly correlated with left temporal and right frontal cortices. Irrespective of domain, delayed memory performance was associated with a network including rather frontal association cortices. Conclusions: The findings demonstrate that neuropsychological deficits as assessed by the CERAD involve different cerebral sites and thus underline the clinical validity of this clinical instrument.