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Lewy body disease (LBD) is characterized by \u03b1-synuclein aggregates in the form of Lewy bodies as well as the deposition of extracellular amyloid plaques, with many cases also exhibiting neurofibrillary tangle (NFT) pathology. In contrast, AD is characterized by amyloid plaques and neurofibrillary tangles. Both conditions often co-occur with additional neuropathological changes, such as vascular disease and TDP-43 pathology.<\/jats:p>\n               <jats:p>To elucidate shared and distinct molecular signatures underlying these mixed neuropathologies, we extensively analysed transcriptional changes in the anterior cingulate cortex, a brain region critically involved in cognitive processes. We performed bulk tissue RNA sequencing from the anterior cingulate cortex and determined differentially expressed genes (q-value &amp;lt;0.05) in control (n = 81), LBD (n = 436), AD (n = 53) and pathological amyloid cases consisting of amyloid pathology with minimal or no tau pathology (n = 39). We used gene set enrichment and weighted gene correlation network analysis to understand the pathways associated with each neuropathologically defined group.<\/jats:p>\n               <jats:p>LBD cases had strong upregulation of inflammatory pathways and downregulation of metabolic pathways. The LBD cases were further subdivided into either high Thal amyloid, Braak NFT, or low pathological burden cohorts. Compared to the control cases, the LBD cohorts consistently showed upregulation for genes involved in protein folding and cytokine immune response, as well as downregulation of fatty acid metabolism. Surprisingly, concomitant tau pathology within the LBD cases resulted in no additional changes. Some core inflammatory pathways were shared between AD and LBD but with numerous disease-specific changes. Direct comparison of LBD cohorts versus AD cases revealed strong enrichment of synaptic signalling, behaviour and neuronal system pathways. Females had a stronger response overall in both LBD and AD, with several sex-specific changes.<\/jats:p>\n               <jats:p>Overall, the results identify genes commonly and uniquely dysregulated in neuropathologically defined LBD and AD cases, shedding light on shared and distinct molecular pathways. Additionally, the study underscores the importance of considering sex-specific changes in understanding the complex transcriptional landscape of these neurodegenerative diseases.<\/jats:p>","DOI":"10.1093\/brain\/awae202","type":"journal-article","created":{"date-parts":[[2024,6,25]],"date-time":"2024-06-25T16:47:59Z","timestamp":1719334079000},"page":"69-88","source":"Crossref","is-referenced-by-count":14,"title":["Distinct transcriptional alterations distinguish Lewy body disease from Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"148","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8578-2069","authenticated-orcid":false,"given":"Kimberly C","family":"Olney","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin E","family":"Rabichow","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]},{"name":"Program in Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aleksandra M","family":"Wojtas","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]},{"name":"Program in Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"DeTure","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pamela J","family":"McLean","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7189-7917","authenticated-orcid":false,"given":"Dennis W","family":"Dickson","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Neurology, University of Arizona , Tucson, AZ 85724 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4813-756X","authenticated-orcid":false,"given":"Owen A","family":"Ross","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Jacksonville, FL 32224 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John D","family":"Fryer","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]},{"name":"Program in Neuroscience, Mayo Clinic , Scottsdale, AZ 85259 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2024,6,25]]},"reference":[{"key":"2025010718551192600_awae202-B1","doi-asserted-by":"crossref","first-page":"6469","DOI":"10.1073\/pnas.95.11.6469","article-title":"alpha-Synuclein in filamentous inclusions of Lewy bodies from Parkinson\u2019s disease and dementia with Lewy bodies","volume":"95","author":"Spillantini","year":"1998","journal-title":"Proc Natl Acad Sci U S A"},{"key":"2025010718551192600_awae202-B2","doi-asserted-by":"crossref","first-page":"1113","DOI":"10.1212\/WNL.47.5.1113","article-title":"Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the consortium on DLB international 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