Back to Authors

Montine, Thomas J.

https://orcid.org/0000-0002-1346-2728

A5067728043 | I4210105618

Mayo Clinic

Alzheimer’s Disease Neuroimaging Initiative

Citations 25

Reply: LATE to the PART-y

Brain | July 19, 2019 | Volume: 142 | Issue: 9 | Pages: e48-e48

10.1093/brain/awz226 | PMID 31359039

Limbic-predominant age-related TDP-43 encephalopathy (LATE): consensus working group report

Brain | March 22, 2019 | Volume: 142 | Issue: 6 | Pages: 1503-1527

10.1093/brain/awz099 | PMID 31039256

“Alzheimer's disease” is neither “Alzheimer's clinical syndrome” nor “dementia”

Alzheimer's & Dementia | January 11, 2019 | Volume: 15 | Issue: 1 | Pages: 153-157

10.1016/j.jalz.2018.11.002 | PMID 30642435

P1‐139: THE CONTRIBUTION OF SEX‐SPECIFIC ASSOCIATIONS IN GENETIC STUDIES OF ALZHEIMER'S DISEASE PATHOLOGY

Alzheimer's & Dementia | October 22, 2018 | Volume: 14 | Issue: 7S_Part_6 | Pages: No page available

10.1016/j.jalz.2018.06.142

The National Institute on Aging and the Alzheimer's Association Research Framework for Alzheimer's disease: Perspectives from the Research Roundtable

Alzheimer's & Dementia | April 10, 2018 | Volume: 14 | Issue: 4 | Pages: 563-575

10.1016/j.jalz.2018.03.002 | PMID 29653607

AbstractThe Alzheimer's Association's Research Roundtable met in November 2017 to explore the new National Institute on Aging and the Alzheimer's Association Research Framework for Alzheimer's disease. The meeting allowed experts in the field from academia, industry, and government to provide perspectives on the new National Institute on Aging and the Alzheimer's Association Research Framework. This review will summarize the “A, T, N System” (Amyloid, Tau, and Neurodegeneration) using biomarkers and how this may be applied to clinical research and drug development. In addition, challenges and barriers to the potential adoption of this new framework will be discussed. Finally, future directions for research will be proposed.
Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease

JAMA Neurology | August 29, 2016 | Volume: 73 | Issue: 10 | Pages: 1217

10.1001/jamaneurol.2016.2245 | PMID 27571329

Characterizing Apolipoprotein E ε4 Carriers and Noncarriers With the Clinical Diagnosis of Mild to Moderate Alzheimer Dementia and Minimal β-Amyloid Peptide Plaques

JAMA Neurology | August 24, 2015 | Volume: 72 | Issue: 10 | Pages: 1124

10.1001/jamaneurol.2015.1721 | PMID 26302353

PARK10 is a major locus for sporadic neuropathologically confirmed Parkinson disease

Neurology | February 7, 2015 | Volume: 84 | Issue: 10 | Pages: 972-980

10.1212/wnl.0000000000001332 | PMID 25663231

Cognitive profile of LRRK2‐related Parkinson's disease

Movement Disorders | February 4, 2015 | Volume: 30 | Issue: 5 | Pages: 728-733

10.1002/mds.26161 | PMID 25650144

AbstractBackgroundIncreasing evidence suggests that genetic factors play a role in the variability associated with cognitive performance in Parkinson's disease (PD). Mutations in the LRRK2 gene are the most common cause of monogenic PD; however, the cognitive profile of LRRK2‐related PD is not well‐characterized.MethodsA cohort of 1,447 PD patients enrolled in the PD Cognitive Genetics Consortium was screened for LRRK2 mutations and completed detailed cognitive testing. Associations between mutation carrier status and cognitive test scores were assessed using linear regression models.ResultsLRRK2 mutation carriers (n = 29) demonstrated better performance on the Mini Mental State Examination (P = 0.03) and the Letter‐Number Sequencing Test (P = 0.005). A smaller proportion of LRRK2 carriers were demented (P = 0.03).ConclusionsOur cross‐sectional study demonstrates better performance on certain cognitive tests, as well as lower rates of dementia in LRRK2‐related PD. Future longitudinal studies are needed to determine whether LRRK2 mutation carriers exhibit slower cognitive decline. © 2015 International Parkinson and Movement Disorder Society
Vascular contributions to cognitive impairment and dementia including Alzheimer's disease

Alzheimer's & Dementia | December 12, 2014 | Volume: 11 | Issue: 6 | Pages: 710-717

10.1016/j.jalz.2014.10.008 | PMID 25510382

Abstract Scientific evidence continues to demonstrate the linkage of vascular contributions to cognitive impairment and dementia such as Alzheimer's disease. In December, 2013, the Alzheimer's Association, with scientific input from the National Institute of Neurological Disorders and Stroke and the National Heart, Lung and Blood Institute from the National Institutes of Health, convened scientific experts to discuss the research gaps in our understanding of how vascular factors contribute to Alzheimer's disease and related dementia. This manuscript summarizes the meeting and the resultant discussion, including an outline of next steps needed to move this area of research forward.