Neurodegenerative brain diseases (NBDs) are characterized by cognitive decline and movement impairments caused by neuronal loss in different brain regions. A large fraction of the genetic heritability of NBDs is not explained by the current known mutations. Genome-wide association studies identified novel disease-risk loci, adding to the genetic basis of NBDs. Many of the associated variants reside in noncoding regions with distinct molecular functions. Genetic variation in these regions can alter functions and contribute to disease pathogenesis. Here, we discuss noncoding variants associated with NBDs. Methods for better functional interpretation of noncoding variation will expand our knowledge of the genetic architecture of NBDs and broaden the routes for therapeutic strategies. Until recently, studies focused on the coding part of the genome to explain the genetic basis of neurodegenerative brain diseases (NBDs). However, a large fraction of heritability of NBDs is still missing Genome-wide association studies have identified noncoding variants that are significantly associated with NBDs. Most reside in regulatory regions such as promoters, enhancers, and noncoding RNAs (ncRNAs), which suggests that they might modulate the effect of these elements. Noncoding variants can contribute to disease susceptibility by impacting mRNA processing, modulating long-range chromatin interactions, altering transcription factor binding sites, and regulating ncRNA expression. Intersection of epigenetic with genetic information in diverse cell types could assign functional properties to noncoding variants and elucidate cell-specific effects that are masked in bulk tissue analyses. [ABSTRACT FROM AUTHOR]