<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Miller RL</submitter><funding>National Institute of Neurological Disorders and Stroke</funding><funding>NINDS NIH HHS</funding><funding>Michael J. Fox Foundation for Parkinson&amp;apos;s Research</funding><pagination>106-121</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8862415</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(2)</volume><pubmed_abstract>&lt;h4>Objective&lt;/h4>Parkinson disease (PD) is defined by the accumulation of misfolded α-synuclein (α-syn) in Lewy bodies and Lewy neurites. It affects multiple cortical and subcortical neuronal populations. The majority of people with PD develop dementia, which is associated with Lewy bodies in neocortex and referred to as Lewy body dementia (LBD). Other neuropathologic changes, including amyloid β (Aβ) and tau accumulation, occur in some LBD cases. We sought to quantify α-syn, Aβ, and tau accumulation in neocortical, limbic, and basal ganglia regions.&lt;h4>Methods&lt;/h4>We isolated insoluble protein from fresh frozen postmortem brain tissue samples for eight brains regions from 15 LBD, seven Alzheimer disease (AD), and six control cases. We measured insoluble α-syn, Aβ, and tau with recently d</pubmed_abstract><journal>Annals of clinical and translational neurology</journal><pubmed_title>Quantifying regional α -synuclein, amyloid β, and tau accumulation in lewy body dementia.</pubmed_title><pmcid>PMC8862415</pmcid><funding_grant_id>NS075321</funding_grant_id><funding_grant_id>R01 NS097799</funding_grant_id><funding_grant_id>R01 NS097437</funding_grant_id><funding_grant_id>NS097799</funding_grant_id><funding_grant_id>NS097437</funding_grant_id><funding_grant_id>NS110436</funding_grant_id><pubmed_authors>Liu J</pubmed_authors><pubmed_authors>O'Shea JY</pubmed_authors><pubmed_authors>Cairns NJ</pubmed_authors><pubmed_authors>Campbell MC</pubmed_authors><pubmed_authors>Franklin EE</pubmed_authors><pubmed_authors>Miller RL</pubmed_authors><pubmed_authors>Cirrito JR</pubmed_authors><pubmed_authors>Perlmutter JS</pubmed_authors><pubmed_authors>Buddhala C</pubmed_authors><pubmed_authors>Kotzbauer PT</pubmed_authors><pubmed_authors>Dhavale DD</pubmed_authors><pubmed_authors>Loftin SK</pubmed_authors><pubmed_authors>Andruska KM</pubmed_authors><pubmed_authors>Perrin RJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Quantifying regional α -synuclein, amyloid β, and tau accumulation in lewy body dementia.</name><description>&lt;h4>Objective&lt;/h4>Parkinson disease (PD) is defined by the accumulation of misfolded α-synuclein (α-syn) in Lewy bodies and Lewy neurites. It affects multiple cortical and subcortical neuronal populations. The majority of people with PD develop dementia, which is associated with Lewy bodies in neocortex and referred to as Lewy body dementia (LBD). Other neuropathologic changes, including amyloid β (Aβ) and tau accumulation, occur in some LBD cases. We sought to quantify α-syn, Aβ, and tau accumulation in neocortical, limbic, and basal ganglia regions.&lt;h4>Methods&lt;/h4>We isolated insoluble protein from fresh frozen postmortem brain tissue samples for eight brains regions from 15 LBD, seven Alzheimer disease (AD), and six control cases. We measured insoluble α-syn, Aβ, and tau with recently d</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Feb</publication><modification>2025-04-18T16:35:43.959Z</modification><creation>2025-04-07T03:56:17.645Z</creation></dates><accession>S-EPMC8862415</accession><cross_references><pubmed>35060360</pubmed><doi>10.1002/acn3.51482</doi></cross_references></HashMap>