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1. Self-Administered Gerocognitive Examination: longitudinal cohort testing for the early detection of dementia conversion.

Author

Scharre DW, Chang SI, Nagaraja HN, Wheeler NC, and Kataki M

Subjects
Cohort Studies, Disease Progression, Humans, Mental Status and Dementia Tests, Neuropsychological Tests, Alzheimer Disease diagnosis, Alzheimer Disease psychology, Cognitive Dysfunction diagnosis, Cognitive Dysfunction psychology
Abstract

Background: Significant cognitive changes as individuals' age are not being identified in a timely manner, delaying diagnosis and treatments. Use of brief, multi-domain, self-administered, objective cognitive assessment tools may remove some barriers in assessing and identifying cognitive changes. We compared longitudinal Self-Administered Gerocognitive Examination (SAGE) test scores to non-self-administered Mini-Mental State Examination (MMSE) scores in 5 different diagnostic subgroups., Methods: A cohort study evaluating annual rates of change was performed on 665 consecutive patients from Ohio State University Memory Disorders Clinic. Patients with at least two visits 6 months apart evaluated with SAGE and MMSE and classified according to standard clinical criteria as subjective cognitive decline (SCD), mild cognitive impairment (MCI), or Alzheimer's disease (AD) dementia were included. The pattern of change in SAGE scores was compared to MMSE. One way and repeated measures ANOVA and linear regression models were used., Results: Four hundred twenty-four individuals (40 SCD, 94 MCI non-converters to dementia, 70 MCI converters to dementia (49 to AD dementia and 21 to non-AD dementia), 220 AD dementia) met inclusion criteria. SAGE and MMSE scores declined respectively at annual rates of 1.91 points/year (p < 0.0001) and 1.68 points/year (p < 0.0001) for MCI converters to AD dementia, and 1.82 points/year (p < 0.0001) and 2.38 points/year (p < 0.0001) for AD dementia subjects. SAGE and MMSE scores remained stable for SCD and MCI non-converters. Statistically significant decline from baseline scores in SAGE occurred at least 6 months earlier than MMSE for MCI converters to AD dementia (14.4 vs. 20.4 months), MCI converters to non-AD dementia (14.4 vs. 32.9 months), and AD dementia individuals (8.3 vs. 14.4 months)., Conclusions: SAGE detects MCI conversion to dementia at least 6 months sooner than MMSE. Being self-administered, SAGE also addresses a critical need of removing some barriers in performing cognitive assessments. Limitations of our single-site cohort study include potential referral and sampling biases. Repetitively administering SAGE and identifying stability or decline may provide clinicians with an objective cognitive biomarker impacting evaluation and management choices., (© 2021. The Author(s).)

Published
2021
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2. Paired Studies Comparing Clinical Profiles of Lewy Body Dementia with Alzheimer's and Parkinson's Diseases.

Author

Scharre DW, Chang SI, Nagaraja HN, Park A, Adeli A, Agrawal P, Kloos A, Kegelmeyer D, Linder S, Fritz N, Kostyk SK, and Kataki M

Subjects
Aged, Aged, 80 and over, Alzheimer Disease physiopathology, Cross-Sectional Studies, Diagnosis, Differential, Female, Humans, Lewy Body Disease physiopathology, Male, Memory physiology, Middle Aged, Motor Skills physiology, Neuropsychological Tests, Parkinson Disease physiopathology, Alzheimer Disease diagnosis, Alzheimer Disease psychology, Lewy Body Disease diagnosis, Lewy Body Disease psychology, Parkinson Disease diagnosis, Parkinson Disease psychology
Abstract

Limited data compares clinical profiles of Lewy Body Dementia (LBD) with Alzheimer's disease (AD) and Parkinson's disease (PD). Twenty-one mildly demented ambulatory LBD subjects were individually matched by MMSE score with 21 AD subjects and by UPDRS motor score with 21 PD subjects. Matched by age, gender, education, and race, pairs were compared using cognitive, functional, behavioral, and motor measures. LBD group performed worse than PD on axial motor, gait, and balance measures. AD had more amnesia and orientation impairments, but less executive and visuospatial deficits than LBD subjects. LBD group had more sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea than AD or PD. Axial motor, gait, and balance disturbances correlated with executive, visuospatial, and global cognition deficits. LBD is differentiated from AD and PD by retrieval memory, visuospatial, and executive deficits; axial motor, gait and balance impairments; sleepiness, cognitive/behavioral fluctuations, hallucinations, and sleep apnea.

Published
2016
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3. Motor performance differentiates individuals with Lewy body dementia, Parkinson's and Alzheimer's disease.

Author

Fritz NE, Kegelmeyer DA, Kloos AD, Linder S, Park A, Kataki M, Adeli A, Agrawal P, Scharre DW, and Kostyk SK

Subjects
Aged, Aged, 80 and over, Alzheimer Disease diagnosis, Cross-Sectional Studies, Diagnosis, Differential, Female, Humans, Lewy Body Disease diagnosis, Male, Parkinson Disease diagnosis, Alzheimer Disease physiopathology, Gait, Lewy Body Disease physiopathology, Motor Skills, Parkinson Disease physiopathology, Postural Balance
Abstract

Introduction: Differential diagnosis of dementia with Lewy bodies (DLB), Parkinson's disease with dementia (PDD), Parkinson's disease (PD) and Alzheimer's disease (AD) is challenging. Comparative motor profiles of these neurodegenerative disorders may aid in earlier diagnosis but have not been extensively studied., Methods: Groups were rigorously matched by age, education, and sex. DLB/PDD participants were matched by Mini-Mental State Examination Score to individuals with AD and by Unified Parkinson's Disease Rating Scale motor scores to individuals with PD. Gait, balance, dual task walking and hand dexterity measures were compared between a combined group (n=21) of individuals with Lewy body dementia (LBD) consisting of those with DLB (n=11) and PDD (n=10) to individuals with PD (n=21) or AD (n=21)., Results: Individuals at the same disease stage with LBD walked significantly slower with shorter stride lengths (p<0.05), demonstrated poorer balance on both the Tinetti and Berg Balance Scale, and poorer performance on dual-task and figure-of-eight walking compared to PD and AD (p<0.05 for all) groups. Upper extremity coordination on the 9-hole peg test differentiated LBD from both PD and AD and was the only motor test in which individuals with AD performed worse than those with PD. Tinetti balance subscores were significantly lower in PDD compared to DLB participants (10.4±2.3 versus 12.8±2.3; p=0.027)., Conclusions: Motor features distinguish individuals with LBD from those with AD and PD. Measures of gait, balance and finger dexterity provide an additional means of differentiating individuals with LBD from those with AD and PD., (Copyright © 2016 Elsevier B.V. All rights reserved.)

Published
2016
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4. Allelic mRNA expression of sortilin-1 (SORL1) mRNA in Alzheimer's autopsy brain tissues.

Author

Alachkar H, Kataki M, Scharre DW, Papp A, and Sadee W

Subjects
Aged, Autopsy methods, Female, Gene Frequency, Genotype, Humans, Male, Middle Aged, Adaptor Proteins, Vesicular Transport genetics, Alzheimer Disease genetics, Alzheimer Disease metabolism, Alzheimer Disease pathology, Brain metabolism, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide genetics, RNA, Messenger metabolism
Abstract

Polymorphisms in the gene encoding SORL1, involved in cellular trafficking of APP, have been implicated in late-onset Alzheimer's disease, by a mechanism thought to affect mRNA expression. To search for regulatory polymorphisms, we have measured allele-specific mRNA expression of SORL1 in human autopsy tissues from the prefrontal cortex of 26 Alzheimer's patients, and 51 controls, using two synonymous marker SNPs (rs3824968 in exon 34 (11 heterozygous AD subjects and 16 controls), and rs12364988 in exon 6 (8 heterozygous AD subjects)). Significant allelic expression imbalance (AEI), indicative of the presence of cis-acting regulatory factors, was detected in a single control subject, while allelic ratios were near unity for all other subjects. We genotyped 7 SNPs in two haplotype blocks that had previously been implicated in Alzheimer's disease. Since each of these SNPs was heterozygous in several subjects lacking AEI, this study fails to support a regulatory role for SORL1 polymorphisms in mRNA expression.

Published
2008
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5. A method for estimating duration of illness in Alzheimer's disease.

Author

Doody RS, Dunn JK, Huang E, Azher S, and Kataki M

Subjects
Age of Onset, Aged, Caregivers, Disease Progression, Humans, Interviews as Topic, Alzheimer Disease diagnosis, Geriatrics methods, Medical History Taking
Abstract

Background: We developed a set of questions for generating an estimate regarding the date of first symptoms to the nearest half-year. Physicians then revised this estimate in conjunction with medical record review and patient/informant interviews, and by testing the estimate by recall of life events. One experienced examiner rated 36 patients, and each was independently rated by a second, less experienced rater. The physician ratings were compared to each other and to an unstructured caregiver estimate of duration using Lin concordance coefficients. There was excellent agreement between independent physician raters (rho = 0.95, p < 0.001). Caregiver estimates of duration were usually shorter because of failure to relate the first symptoms to the onset of disease., (Copyright 2004 S. Karger AG, Basel)

Published
2004
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6. A blood-based signature of cerebrospinal fluid A beta(1-42) status

Author

Goudey, B., Fung, B.J., Schieber, C., Faux, N.G., Weiner, M.W., Aisen, P., Petersen, R., Jack, C.R., Jagust, W., Trojanowki, J.Q., Toga, A.W., Beckett, L., Green, R.C., Saykin, A.J., Morris, J., Shaw, L.M., Kaye, J., Quinn, J., Silbert, L., Lind, B., Carter, R., Dolen, S., Schneider, L.S., Pawluczyk, S., Beccera, M., Teodoro, L., Spann, B.M., Brewer, J., Vanderswag, H., Fleisher, A., Heidebrink, J.L., Lord, J.L., Mason, S.S., Albers, C.S., Knopman, D., Johnson, K., Doody, R.S., Villanueva-Meyer, J., Chowdhury, M., Rountree, S., Dang, M., Stern, Y., Honig, L.S., Bell, K.L., Ances, B., Morris, J.C., Carroll, M., Creech, M.L., Franklin, E., Mintun, M.A., Schneider, S., Oliver, A., Marson, D., Griffth, R., Clark, D., Geldmacher, D., Brockington, J., Roberson, E., Natelson Love, M., Grossman, H., Mitsis, E., Shah, R.C., deToledo-Morrell, L., Duara, R., Varon, D., Greig, M.T., Roberts, P., Albert, M., Onyike, C., D'Agostino, D., Kielb, S., Galvin, J.E., Cerbone, B., Michel, C.A., Pogorelec, D.M., Rusinek, H., Leon, M.J. de, Glodzik, L., De Santi, S., Doraiswamy, P.M., Petrella, J.R., Borges-Neto, S., Wong, T.Z., Coleman, E., Smith, C.D., Jicha, G., Hardy, P., Sinha, P., Oates, E., Conrad, G., Porsteinsson, A.P., Goldstein, B.S., Martin, K., Makino, K.M., Ismail, M.S., Brand, C., Mulnard, R.A., Thai, G., McAdams-Ortiz, C., Womack, K., Mathews, D., Quiceno, M., Levey, A.I., Lah, J.J., Cellar, J.S., Burns, J.M., Swerdlow, R.H., Brooks, W.M., Apostolova, L., Tingus, K., Woo, E., Silverman, D.H.S., Lu, P.H., Bartzokis, G., Graff-Radford, N.R., Parftt, F., Kendall, T., Johnson, H., Farlow, M.R., Hake, A.M., Matthews, B.R., Brosch, J.R., Herring, S., Hunt, C., Dyck, .H. van, Carson, R.E., MacAvoy, M.G., Varma, P., Chertkow, H., Bergman, H., Hosein, C., Black, S., Stefanovic, B., Caldwell, C., Hsiung, Ging-Yuek Robin, Feldman, H., Mudge, B., Assaly, M., Finger, E., Pasternack, S., Rachisky, I., Trost, D., Kertesz, A., Bernick, C., Munic, D., Mesulam, M.-M., Lipowski, K., Weintraub, S., Bonakdarpour, B., Kerwin, D., Wu, C.-K., Johnson, N., Sadowsky, C., Villena, T., Turner, R.S., Reynolds, B., Sperling, R.A., Johnson, K.A., Marshall, G., Yesavage, J., Taylor, J.L., Lane, B., Rosen, A., Tinklenberg, J., Sabbagh, M.N., Belden, C.M., Jacobson, S.A., Sirrel, S.A., Kowall, N., Killiany, R., Budson, A.E., Norbash, A., Johnson, P.L., Obisesan, T.O., Wolday, S., Allard, J., Lerner, A., Ogrocki, P., Tatsuoka, C., Fatica, P., Fletcher, E., Maillard, P., Olichney, J., DeCarli, C., Carmichael, O., Kittur, S., Borrie, M., Lee, T.-Y., Bartha, R., Johnson, S., Asthana, S., Carlsson, C.M., Potkin, S.G., Preda, A., Nguyen, D., Tariot, P., Burke, A., Trncic, N., Reeder, S., Bates, V., Capote, H., Rainka, M., Scharre, D.W., Kataki, M., Adeli, A., Zimmerman, E.A., Celmins, D., Brown, A.D., Pearlson, G.D., Blank, K., Anderson, K., Flashman, L.A., Seltzer, M., Hynes, M.L., Santulli, R.B., Sink, K.M., Gordineer, L., Williamson, J.D., Garg, P., Watkins, F., Ott, B.R., Querfurth, H., Tremont, G., Salloway, S., Malloy, P., Correia, S., Rosen, H.J., Miller, B.L., Perry, D., Mintzer, J., Spicer, K., Bachman, D., Pomara, N., Hernando, R., Sarrael, A., Relkin, N., Chaing, G., Lin, M., Ravdin, L., Smith, A., Raj, B.A., Fargher, K., Saykin, A., Nho, K., Kling, M., Toledo, J., Shaw, L., Trojanowski, J., Farrer, L., Kastsenmueller, G., Arnold, M., Wishart, D., Wurtz, P., Bhattcharyya, S., Duijin, C. van, Mangravite, L., Han, X., Hankemeier, T., Fiehn, O., Barupal, D., Thiele, I., Heinken, A., Meikle, P., Price, N., Funk, C., Jia, W., Kueider-Paisley, A., Tenebaum, J., Black, C., Moseley, A., Thompson, W., Mahmoudiandehkorki, S., Baillie, R., Welsh-Bohmer, K., Plassman, B., and Epidemiology

Subjects
Male, 0301 basic medicine, Apolipoprotein E, Oncology, medicine.medical_specialty, Amyloid, Amyloid beta, lcsh:Medicine, Article, 03 medical and health sciences, Apolipoproteins E, 0302 clinical medicine, Cerebrospinal fluid, Alzheimer Disease, Predictive Value of Tests, Internal medicine, medicine, Humans, Dementia, Cognitive decline, lcsh:Science, Aged, Aged, 80 and over, Amyloid beta-Peptides, Multidisciplinary, biology, Chemokine CCL26, business.industry, lcsh:R, Alzheimer’s Disease Metabolomics Consortium, Alzheimer’s Disease Neuroimaging Initiative, medicine.disease, Peptide Fragments, 3. Good health, 030104 developmental biology, biology.protein, Chromogranin A, Female, lcsh:Q, Alzheimer's disease, business, Biomarkers, 030217 neurology & neurosurgery, Alzheimer's Disease Neuroimaging Initiative
Abstract

It is increasingly recognized that Alzheimer’s disease (AD) exists before dementia is present and that shifts in amyloid beta occur long before clinical symptoms can be detected. Early detection of these molecular changes is a key aspect for the success of interventions aimed at slowing down rates of cognitive decline. Recent evidence indicates that of the two established methods for measuring amyloid, a decrease in cerebrospinal fluid (CSF) amyloid β1−42 (Aβ1−42) may be an earlier indicator of Alzheimer’s disease risk than measures of amyloid obtained from Positron Emission Tomography (PET). However, CSF collection is highly invasive and expensive. In contrast, blood collection is routinely performed, minimally invasive and cheap. In this work, we develop a blood-based signature that can provide a cheap and minimally invasive estimation of an individual’s CSF amyloid status using a machine learning approach. We show that a Random Forest model derived from plasma analytes can accurately predict subjects as having abnormal (low) CSF Aβ1−42 levels indicative of AD risk (0.84 AUC, 0.78 sensitivity, and 0.73 specificity). Refinement of the modeling indicates that only APOEε4 carrier status and four plasma analytes (CGA, Aβ1−42, Eotaxin 3, APOE) are required to achieve a high level of accuracy. Furthermore, we show across an independent validation cohort that individuals with predicted abnormal CSF Aβ1−42 levels transitioned to an AD diagnosis over 120 months significantly faster than those with predicted normal CSF Aβ1−42 levels and that the resulting model also validates reasonably across PET Aβ1−42 status (0.78 AUC). This is the first study to show that a machine learning approach, using plasma protein levels, age and APOEε4 carrier status, is able to predict CSF Aβ1−42 status, the earliest risk indicator for AD, with high accuracy.

Published
2019

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