Carol F. Lippa
Thomas Jefferson University
PsychiatryInternal medicinePathologyPsychologyNeuroscienceCognitionPresenilinPediatricsDegenerative diseaseDementia with Lewy bodiesFrontotemporal dementiaLewy bodyDiseaseDementiaMutationAlzheimer's diseaseGeneticsMedicineGerontologyBiology
187Publications
50H-index
11.1kCitations
Publications 184
Newest
#1James B. Leverenz (Cleveland Clinic)H-Index: 83
#2Lynn M. Bekris (Cleveland Clinic)H-Index: 10
Last. Cyrus P. Zabetian (UW: University of Washington)H-Index: 67
view all 16 authors...
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#1Jennifer G. Goldman (NU: Northwestern University)H-Index: 40
#2Leah K. Forsberg (Mayo Clinic)H-Index: 8
Last. Todd GrahamH-Index: 2
view all 20 authors...
Lewy body dementia (LBD), including dementia with Lewy bodies and Parkinson’s disease dementia, affects over a million people in the USA and has a substantial impact on patients, caregivers, and society. Symptomatic treatments for LBD, which can include cognitive, neuropsychiatric, autonomic, sleep, and motor features, are limited with only two drugs (cholinesterase inhibitors) currently approved by regulatory agencies for dementia in LBD. Clinical trials represent a top research priority, but t...
1 CitationsSource
#1Yu Ding (Nanjing University of Chinese Medicine)H-Index: 2
#2Jiahui Zhao (Nanjing University of Chinese Medicine)H-Index: 2
Last. Yuesong Gong (Drexel University)H-Index: 9
view all 10 authors...
Background: β-Amyloid protein (Aβ) putatively plays a seminal role in synaptic loss in Alzheimer’s disease (AD). While there is no consensus regarding the synaptic-relevant species of Aβ, it is known that Aβ oligomers (AβOs) are noticeably increased in the early stages of AD, localizing at or within the synapse. In cell and animal models, AβOs have been shown to attach to synapses and instigate synapse dysfunction and deterioration. To establish the pathological mechanism of synaptic loss in AD,...
19 CitationsSource
#1Jason C. You (Thomas Jefferson University)H-Index: 5
#2Erica Jones (Thomas Jefferson University Hospital)H-Index: 1
Last. Carol F. Lippa (Thomas Jefferson University Hospital)H-Index: 50
view all 7 authors...
Importance Evidence shows that sleep dysfunction and β-amyloid (Aβ) deposition work synergistically to impair brain function in individuals with normal cognition, increasing the risk of developing dementia later in life. However, whether Aβ continues to play an integral role in sleep dysfunction after the onset of cognitive decline in individuals with dementia is unclear. Objective To determine whether Aβ deposition in the brain is associated with subjective measures of sleep quality and cogniti...
3 CitationsSource
#1Bethany PetersonH-Index: 1
#2Melissa J. Armstrong (UF: University of Florida)H-Index: 27
Last. Brad F. Boeve (Mayo Clinic)H-Index: 15
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The first Lewy Body Dementia Association (LBDA) Research Centers of Excellence (RCOE) Investigator’s meeting was held on December 14, 2017, in New Orleans. The program was established to increase patient access to clinical experts on Lewy body dementia (LBD), which includes dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), and to create a clinical trials-ready network. Four working groups (WG) were created to pursue the LBDA RCOE aims: (1) increase access to high-quality cl...
3 CitationsSource
#1James B. Leverenz (Cleveland Clinic)H-Index: 83
#2Sarah B. Berman (University of Pittsburgh)H-Index: 22
Last. Cyrus P. ZabetianH-Index: 67
view all 14 authors...
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#1Bradley F. BoeveH-Index: 137
Last. Angela E TaylorH-Index: 27
view all 45 authors...
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#1Cyril Pottier (Mayo Clinic)H-Index: 19
#2Xiaolai Zhou (Mayo Clinic)H-Index: 15
Last. Rosa Rademakers (Mayo Clinic)H-Index: 9
view all 133 authors...
Summary Background Loss-of-function mutations in GRN cause frontotemporal lobar degeneration (FTLD). Patients with GRN mutations present with a uniform subtype of TAR DNA-binding protein 43 (TDP-43) pathology at autopsy (FTLD-TDP type A); however, age at onset and clinical presentation are variable, even within families. We aimed to identify potential genetic modifiers of disease onset and disease risk in GRN mutation carriers. Methods The study was done in three stages: a discovery stage, a rep...
48 CitationsSource
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#1Ian R. A. Mackenzie (UBC: University of British Columbia)H-Index: 94
#2Alexandra M. Nicholson (Mayo Clinic)H-Index: 16
Last. Rosa Rademakers (Mayo Clinic)H-Index: 103
view all 42 authors...
Summary Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are age-related neurodegenerative disorders with shared genetic etiologies and overlapping clinical and pathological features. Here we studied a novel ALS/FTD family and identified the P362L mutation in the low-complexity domain (LCD) of T cell-restricted intracellular antigen-1 (TIA1). Subsequent genetic association analyses showed an increased burden of TIA1 LCD mutations in ALS patients compared to controls (p = 8.7...
280 CitationsSource