Better cardiovascular health is associated with slowed clinical progression in autosomal dominant frontotemporal lobar degeneration variant carriers.

Autor: VandeBunte AM; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA.; Department of Psychology, Palo Alto University, Palo Alto, California, United States., Lee H; Division of Neurology, UBC Hospital, University of British Columbia, Vancouver, British Columbia, Canada., Paolillo EW; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Hsiung GR; Division of Neurology, UBC Hospital, University of British Columbia, Vancouver, British Columbia, Canada., Staffaroni AM; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Saloner R; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Tartaglia C; Tanz Centre for Research in Neurodegenerative Diseases, Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada., Yaffe K; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Knopman DS; Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA., Ramos EM; David Geffen School of Medicine at UCLA, UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, California, USA., Rascovsky K; Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, USA., Bozoki AC; Department of Neurology, University of North Carolina, Chapel Hill, North Carolina, USA., Wong B; Harvard Massachusetts General Hospital Frontotemporal Disorders Unit, Charlestown, Massachusetts, USA., Domoto-Reilly K; Department of Neurology, University of Washington, Seattle, Washington, USA., Snyder A; National Institute of Neurological Disorders and Stroke, Bethesda, Maryland, USA., Pressman P; Department of Neurology, University of Colorado School of Medicine, Aurora, Colorado, USA., Mendez MF; David Geffen School of Medicine at UCLA, Reed Neurological Research Center, Los Angeles, California, USA., Litvan I; San Diego Department of Neurosciences, University of California, San Diego, La Jolla, California, USA., Fields JA; Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA., Galasko DR; San Diego Department of Neurosciences, University of California, San Diego, La Jolla, California, USA., Darby R; Department of Neurology, Vanderbilt University, Nashville, Tennessee, USA., Masdeu JC; Houston Methodist Neurological Institute, Houston, Texas, USA., Pasqual MB; Houston Methodist Neurological Institute, Houston, Texas, USA., Honig LS; Department of Neurology, Irving Medical Center, Columbia University, New York, New York, USA., Ghoshal N; Department of Neurology, St. Louis School of Medicine, Washington University, St. Louis, Missouri, USA., Appleby BS; Department of Neurology, Case Western Reserve University, Cleveland, Ohio, USA., Mackenzie IR; Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, British Columbia, Canada., Heuer HW; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Kramer JH; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Boxer AL; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Forsberg LK; Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA., Boeve B; Department of Neurology, Mayo Clinic, Rochester, Minnesota, USA., Rosen HJ; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA., Casaletto KB; Department of Neurology, University of California, San Francisco, Memory and Aging Center, San Francisco, California, USA.
Jazyk: angličtina
Zdroj: Alzheimer's & dementia : the journal of the Alzheimer's Association [Alzheimers Dement] 2024 Oct; Vol. 20 (10), pp. 6820-6833. Date of Electronic Publication: 2024 Sep 06.
DOI: 10.1002/alz.14172
Abstrakt: Introduction: Cardiovascular health is important for brain aging, yet its role in the clinical manifestation of autosomal dominant or atypical forms of dementia has not been fully elucidated. We examined relationships between Life's Simple 7 (LS7) and clinical trajectories in individuals with autosomal dominant frontotemporal lobar degeneration (FTLD).
Methods: Two hundred forty-seven adults carrying FTLD pathogenic genetic variants (53% asymptomatic) and 189 non-carrier controls completed baseline LS7, and longitudinal neuroimaging and neuropsychological testing.
Results: Among variant carriers, higher baseline LS7 is associated with slower accumulation of frontal white matter hyperintensities (WMHs), as well as slower memory and language declines. Higher baseline LS7 associated with larger baseline frontotemporal volume, but not frontotemporal volume trajectories.
Discussion: Better baseline cardiovascular health related to slower cognitive decline and accumulation of frontal WMHs in autosomal dominant FTLD. Optimizing cardiovascular health may be an important modifiable approach to bolster cognitive health and brain integrity in FTLD.
Highlights: Better cardiovascular health associates with slower cognitive decline in frontotemporal lobar degeneration (FTLD). Lifestyle relates to the accumulation of frontal white matter hyperintensities in FTLD. More optimal cardiovascular health associates with greater baseline frontotemporal lobe volume. Optimized cardiovascular health relates to more favorable outcomes in genetic dementia.
(© 2024 The Author(s). Alzheimer's & Dementia published by Wiley Periodicals LLC on behalf of Alzheimer's Association.)
Databáze: MEDLINE
Externí odkaz: