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We analyzed clinical features and compared FDG\u2010PET metabolism in LPA\u2010DLBD to an independent group of patients with clinical pDLB and regional \u03b1\u2010synuclein burden on digital pathology to a second independent group of autopsied patients with DLBD pathology and antemortem pDLB (DLB\u2010DLBD).<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>All patients with LPA\u2010DLBD were men. Neurological, speech, and neuropsychological characteristics were similar across LPA\u2010DLBD, LPA\u2010Alzheimer's disease (LPA\u2010AD), and LPA\u2010frontotemporal lobar degeneration (LPA\u2010FTLD). Genetic screening of AD, DLBD, and FTLD linked genes were negative with the exception of <jats:italic>APOE \u03b54<\/jats:italic> allele present in 83% of LPA\u2010DLBD patients. Seventy\u2010five percent of the patients with LPA\u2010DLBD showed a parietal\u2010dominant pattern of hy pometabolism; LPA\u2010FTLD \u2013 temporal\u2010dominant pattern, whereas LPA\u2010AD showed heterogeneous patterns of hypometabolism. LPA\u2010DLBD had more asymmetrical hypometabolism affecting frontal lobes, with relatively spared occipital lobe in the nondominantly affected hemisphere, compared to pDLB. LPA\u2010DLBD had minimal atrophy on gross brain examination, higher cortical Lewy body counts, and higher \u03b1\u2010synuclein burden in the middle frontal and inferior parietal cortices compared to DLB\u2010DLBD.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>Whereas AD is the most frequent underlying pathology of LPA, DLBD can also be present and may contribute to the LPA phenotype possibly due to \u03b1\u2010synuclein\u2010associated functional impairment of the dominant parietal lobe. 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