A comprehensive meta-analysis of 130 FDG-PET studies encompassing 5,412 individuals with age-associated neurodegenerative diseases and 3,549 controls identified both decreased and increased brain glucose metabolism as universal features across Alzheimer's, Parkinson's, ALS, and multiple sclerosis. Each disease displayed unique neuroanatomical metabolic signatures, with hypermetabolic regions potentially representing adaptive neural compensation rather than pathology. This finding challenges the traditional focus on glucose hypometabolism in neurodegeneration research. The discovery of disease-specific yet overlapping glucose dysregulation patterns suggests the brain actively remodels its bioenergetic systems in response to neurodegenerative processes. These adaptive responses may represent therapeutic targets for preserving cognitive and motor function. However, this preprint awaits peer review, and the clinical significance of hypermetabolic regions requires validation through longitudinal studies. The research provides a foundational framework for understanding how brain energy metabolism responds to neurodegeneration, potentially informing precision medicine approaches. While the large sample size strengthens these findings, the cross-sectional nature limits causal interpretations about whether metabolic changes drive or result from neurodegeneration.