BACKGROUND: The pathologic outcome of patients diagnosed with mild cognitive impairment (MCI) following progression to dementia is poorly understood. OBJECTIVE: To determine the pathologic substrates of dementia in cases with prior diagnosis of amnestic MCI. DESIGN AND SETTING: Community-based cohort. PATIENTS: Thirty-four subjects followed up prospectively as part of a community-based study who were diagnosed with amnestic MCI, progressed to clinical dementia, and underwent subsequent postmortem brain analysis. MAIN OUTCOME MEASURES: Neuropathologic analyses resulted in assignment of a primary pathologic diagnosis and included staging of Alzheimer pathologic abnormalities and identification of contributing vascular disease, Lewy bodies, and argyrophilic grains. RESULTS: Although the majority of subjects progressed both clinically and pathologically to Alzheimer disease (AD), 10 (29%) of them developed non-AD primary pathologic abnormalities. All of the cases were found to have sufficient pathologic abnormalities in mesial temporal lobe structures to account for their amnestic symptoms regardless of the cause. Most subjects were found to have secondary contributing pathologic abnormalities in addition to primary pathologic diagnoses. No significant differences between subjects with and without neuropathologically proven AD were detected in demographic variables, apolipoprotein E genotype, or cognitive test measures at onset of MCI, onset of dementia, or last clinical evaluation. CONCLUSIONS: The neuropathologic outcome of amnestic MCI following progression to dementia is heterogeneous, and it includes AD at a high frequency. Complex neuropathologic findings including 2 or more distinct pathologic entities contributing to dementia may be common in community-based cohorts. Neither demographic variables nor cognitive measures had predictive value in determining which patients diagnosed with MCI will develop the neuropathologic features of AD.
BACKGROUND: The pathologic outcome of patients diagnosed with mild cognitive impairment (MCI) following progression to dementia is poorly understood. OBJECTIVE: To determine the pathologic substrates of dementia in cases with prior diagnosis of amnestic MCI. DESIGN AND SETTING: Community-based cohort. PATIENTS: Thirty-four subjects followed up prospectively as part of a community-based study who were diagnosed with amnestic MCI, progressed to clinical dementia, and underwent subsequent postmortem brain analysis. MAIN OUTCOME MEASURES: Neuropathologic analyses resulted in assignment of a primary pathologic diagnosis and included staging of Alzheimer pathologic abnormalities and identification of contributing vascular disease, Lewy bodies, and argyrophilic grains. RESULTS: Although the majority of subjects progressed both clinically and pathologically to Alzheimer disease (AD), 10 (29%) of them developed non-AD primary pathologic abnormalities. All of the cases were found to have sufficient pathologic abnormalities in mesial temporal lobe structures to account for their amnestic symptoms regardless of the cause. Most subjects were found to have secondary contributing pathologic abnormalities in addition to primary pathologic diagnoses. No significant differences between subjects with and without neuropathologically proven AD were detected in demographic variables, apolipoprotein E genotype, or cognitive test measures at onset of MCI, onset of dementia, or last clinical evaluation. CONCLUSIONS: The neuropathologic outcome of amnestic MCI following progression to dementia is heterogeneous, and it includes AD at a high frequency. Complex neuropathologic findings including 2 or more distinct pathologic entities contributing to dementia may be common in community-based cohorts. Neither demographic variables nor cognitive measures had predictive value in determining which patients diagnosed with MCI will develop the neuropathologic features of AD.
Authors: Liana G Apostolova; Kristy S Hwang; John P Andrawis; Amity E Green; Sona Babakchanian; Jonathan H Morra; Jeffrey L Cummings; Arthur W Toga; John Q Trojanowski; Leslie M Shaw; Clifford R Jack; Ronald C Petersen; Paul S Aisen; William J Jagust; Robert A Koeppe; Chester A Mathis; Michael W Weiner; Paul M Thompson Journal: Neurobiol Aging Date: 2010-06-11 Impact factor: 4.673
Authors: Clifford R Jack; Marilyn S Albert; David S Knopman; Guy M McKhann; Reisa A Sperling; Maria C Carrillo; Bill Thies; Creighton H Phelps Journal: Alzheimers Dement Date: 2011-04-21 Impact factor: 21.566
Authors: Michelle M Mielke; Ozioma C Okonkwo; Kenichi Oishi; Susumu Mori; Sarah Tighe; Michael I Miller; Can Ceritoglu; Timothy Brown; Marilyn Albert; Constantine G Lyketsos Journal: Alzheimers Dement Date: 2012 Impact factor: 21.566
Authors: Katherine J Bangen; Amy J Jak; Dawn M Schiehser; Lisa Delano-Wood; Elizabeth Tuminello; S Duke Han; Dean C Delis; Mark W Bondi Journal: J Int Neuropsychol Soc Date: 2010-04-07 Impact factor: 2.892
Authors: Terry E Goldberg; Jeremy Koppel; Lynda Keehlisen; Erica Christen; Ute Dreses-Werringloer; Concepcion Conejero-Goldberg; Marc L Gordon; Peter Davies Journal: Am J Psychiatry Date: 2010-04-01 Impact factor: 18.112
Authors: Peng Yu; Jia Sun; Robin Wolz; Diane Stephenson; James Brewer; Nick C Fox; Patricia E Cole; Clifford R Jack; Derek L G Hill; Adam J Schwarz Journal: Neurobiol Aging Date: 2013-10-03 Impact factor: 4.673