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Article ; Online: A novel CSF1R variant in a South Dakota family with CSF1R-related leukoencephalopathy.

Ali, Shan / Tipton, Philip W / Koga, Shunsuke / Middlebrooks, Erik H / Josephs, Keith A / Strongosky, Audrey / Dickson, Dennis W / Wszolek, Zbigniew K

Parkinsonism & related disorders

2022 Volume 102, Page(s) 51–53

MeSH term(s)	Humans ; Leukoencephalopathies/genetics ; Mutation ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; South Dakota
Chemical Substances	Receptors, Granulocyte-Macrophage Colony-Stimulating Factor
Language	English
Publishing date	2022-07-31
Publishing country	England
Document type	Letter ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1311489-x
ISSN	1873-5126 ; 1353-8020
ISSN (online)	1873-5126
ISSN	1353-8020
DOI	10.1016/j.parkreldis.2022.07.016
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Zs.A 4553: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Cancer in pathologically confirmed multiple system atrophy.

Cheshire, William P / Koga, Shunsuke / Tipton, Philip W / Sekiya, Hiroaki / Ross, Owen A / Uitti, Ryan J / Josephs, Keith A / Dickson, Dennis W

Clinical autonomic research : official journal of the Clinical Autonomic Research Society

2023 Volume 33, Issue 4, Page(s) 451–458

Abstract: Purpose: The aim of this study was to assess whether cancer occurs with increased frequency in multiple system atrophy (MSA). The pathological hallmark of MSA is glial cytoplasmic inclusions containing aggregated α-synuclein, and the related protein γ- ... ...

Abstract	Purpose: The aim of this study was to assess whether cancer occurs with increased frequency in multiple system atrophy (MSA). The pathological hallmark of MSA is glial cytoplasmic inclusions containing aggregated α-synuclein, and the related protein γ-synuclein correlates with invasive cancer. We investigated whether these two disorders are associated clinically. Methods: Medical records of 320 patients with pathologically confirmed MSA seen between 1998 and 2022 were reviewed. After excluding those with insufficient medical histories, the remaining 269 and an equal number of controls matched for age and sex were queried for personal and family histories of cancer recorded on standardized questionnaires and in clinical histories. Additionally, age-adjusted rates of breast cancer were compared with US population incidence data. Results: Of 269 cases in each group, 37 with MSA versus 45 of controls had a personal history of cancer. Reported cases of cancer in parents were 97 versus 104 and in siblings 31 versus 44 for MSA and controls, respectively. Of 134 female cases in each group, 14 MSA versus 10 controls had a personal history of breast cancer. The age-adjusted rate of breast cancer in MSA was 0.83%, as compared with 0.67% in controls and 2.0% in the US population. All comparisons were nonsignificant. Conclusion: The evidence from this retrospective cohort found no significant clinical association of MSA with breast cancer or other cancers. These results do not exclude the possibility that knowledge about synuclein pathology at the molecular level in cancer may lead to future discoveries and potential therapeutic targets for MSA.
MeSH term(s)	Humans ; Female ; Multiple System Atrophy/metabolism ; Retrospective Studies ; alpha-Synuclein/metabolism ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Brain
Chemical Substances	alpha-Synuclein
Language	English
Publishing date	2023-05-13
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1080007-4
ISSN	1619-1560 ; 0959-9851
ISSN (online)	1619-1560
ISSN	0959-9851
DOI	10.1007/s10286-023-00946-w
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Zs.A 3270: Show issues

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Article ; Online: Progression to corticobasal syndrome: a longitudinal study of patients with nonfluent primary progressive aphasia and primary progressive apraxia of speech.

Garcia-Guaqueta, Danna P / Botha, Hugo / Utianski, Rene L / Duffy, Joseph R / Clark, Heather M / Goodrich, Austin W / Pham, Nha Trang Thu / Machulda, Mary M / Baker, Matt / Rademakers, Rosa / Whitwell, Jennifer L / Josephs, Keith A

Journal of neurology

2024

Abstract: Background and objectives: Nonfluent variant primary progressive aphasia (nfvPPA) and primary progressive apraxia of speech (PPAOS) can be precursors to corticobasal syndrome (CBS). Details on their progression remain unclear. We aimed to examine the ... ...

Abstract	Background and objectives: Nonfluent variant primary progressive aphasia (nfvPPA) and primary progressive apraxia of speech (PPAOS) can be precursors to corticobasal syndrome (CBS). Details on their progression remain unclear. We aimed to examine the clinical and neuroimaging evolution of nfvPPA and PPAOS into CBS. Methods: We conducted a retrospective longitudinal study in 140 nfvPPA or PPAOS patients and applied the consensus criteria for possible and probable CBS for every visit, evaluating limb rigidity, akinesia, limb dystonia, myoclonus, ideomotor apraxia, alien limb phenomenon, and nonverbal oral apraxia (NVOA). Given the association of NVOA with AOS, we also modified the CBS criteria by excluding NVOA and assigned every patient to either a progressors or non-progressors group. We evaluated the frequency of every CBS feature by year from disease onset, and assessed gray and white matter volume loss using SPM12. Results: Asymmetric akinesia, NVOA, and limb apraxia were the most common CBS features that developed; while limb dystonia, myoclonus, and alien limb were rare. Eighty-two patients progressed to possible CBS; only four to probable CBS. nfvPPA and PPAOS had a similar proportion of progressors, although nfvPPA progressed to CBS earlier (p-value = 0.046), driven by an early appearance of limb apraxia (p-value = 0.0041). The non-progressors and progressors both showed premotor/motor cortex involvement at baseline, with spread into prefrontal cortex over time. Discussion: An important proportion of patients with nfvPPA and PPAOS progress to possible CBS, while they rarely develop features of probable CBS even after long follow-up.
Language	English
Publishing date	2024-04-07
Publishing country	Germany
Document type	Journal Article
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-024-12344-x
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Article ; Online: A STAT3 protein complex required for mitochondrial mRNA stability and cancer.

Fernando, C Dilanka / Jayasekara, W Samantha N / Inampudi, Chaitanya / Kohonen-Corish, Maija R J / Cooper, Wendy A / Beilharz, Traude H / Josephs, Tracy M / Garama, Daniel J / Gough, Daniel J

Cell reports

2023 Volume 42, Issue 9, Page(s) 113033

Abstract: Signal transducer and activator of transcription 3 (STAT3) is a potent transcription factor necessary for life whose activity is corrupted in diverse diseases, including cancer. STAT3 biology was presumed to be entirely dependent on its activity as a ... ...

Abstract	Signal transducer and activator of transcription 3 (STAT3) is a potent transcription factor necessary for life whose activity is corrupted in diverse diseases, including cancer. STAT3 biology was presumed to be entirely dependent on its activity as a transcription factor until the discovery of a mitochondrial pool of STAT3, which is necessary for normal tissue function and tumorigenesis. However, the mechanism of this mitochondrial activity remained elusive. This study uses immunoprecipitation and mass spectrometry to identify a complex containing STAT3, leucine-rich pentatricopeptide repeat containing (LRPPRC), and SRA stem-loop-interacting RNA-binding protein (SLIRP) that is required for the stability of mature mitochondrially encoded mRNAs and transport to the mitochondrial ribosome. Moreover, we show that this complex is enriched in patients with lung adenocarcinoma and that its deletion inhibits the growth of lung cancer in vivo, providing therapeutic opportunities through the specific targeting of the mitochondrial activity of STAT3.
MeSH term(s)	Humans ; STAT3 Transcription Factor/genetics ; STAT3 Transcription Factor/metabolism ; Mitochondria/metabolism ; Adenocarcinoma of Lung/metabolism ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; RNA Stability/genetics ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism
Chemical Substances	STAT3 Transcription Factor ; STAT3 protein, human ; SLIRP protein, human ; RNA-Binding Proteins
Language	English
Publishing date	2023-09-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2023.113033
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Article ; Online: Comparison of Clinical, Genetic, and Pathologic Features of Limbic and Diffuse Transactive Response DNA-Binding Protein 43 Pathology in Alzheimer's Disease Neuropathologic Spectrum.

Carlos, Arenn F / Machulda, Mary M / Rutledge, Matthew H / Nguyen, Aivi T / Reichard, R Ross / Baker, Matthew C / Rademakers, Rosa / Dickson, Dennis W / Petersen, Ronald C / Josephs, Keith A

Journal of Alzheimer's disease : JAD

2023 Volume 93, Issue 4, Page(s) 1521–1535

Abstract: ... neuropathologic evaluations. AD-TDP pathology distribution was assessed using the Josephs 6-stage scale. Stages 1 ...

Abstract	Background: Increasing evidence suggests that TAR DNA-binding protein 43 (TDP-43) pathology in Alzheimer's disease (AD), or AD-TDP, can be diffuse or limbic-predominant. Understanding whether diffuse AD-TDP has genetic, clinical, and pathological features that differ from limbic AD-TDP could have clinical and research implications. Objective: To better characterize the clinical and pathologic features of diffuse AD-TDP and differentiate it from limbic AD-TDP. Methods: 363 participants from the Mayo Clinic Study of Aging, Alzheimer's Disease Research Center, and Neurodegenerative Research Group with autopsy confirmed AD and TDP-43 pathology were included. All underwent genetic, clinical, neuropsychologic, and neuropathologic evaluations. AD-TDP pathology distribution was assessed using the Josephs 6-stage scale. Stages 1-3 were classified as Limbic, those 4-6 as Diffuse. Multivariable logistic regression was used to identify clinicopathologic features that independently predicted diffuse pathology. Results: The cohort was 61% female and old at onset (median: 76 years [IQR:70-82]) and death (median: 88 years [IQR:82-92]). Fifty-four percent were Limbic and 46% Diffuse. Clinically, ∼10-20% increases in odds of being Diffuse associated with 5-year increments in age at onset (p = 0.04), 1-year longer disease duration (p = 0.02), and higher Neuropsychiatric Inventory scores (p = 0.03), while 15-second longer Trailmaking Test-B times (p = 0.02) and higher Block Design Test scores (p = 0.02) independently decreased the odds by ~ 10-15%. There was evidence for association of APOEɛ4 allele with limbic AD-TDP and of TMEM106B rs3173615 C allele with diffuse AD-TDP. Pathologically, widespread amyloid-β plaques (Thal phases: 3-5) decreased the odds of diffuse TDP-43 pathology by 80-90%, while hippocampal sclerosis increased it sixfold (p < 0.001). Conclusion: Diffuse AD-TDP shows clinicopathologic and genetic features different from limbic AD-TDP.
MeSH term(s)	Humans ; Female ; Male ; Alzheimer Disease/pathology ; Amyloid beta-Peptides ; Neuropathology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Membrane Proteins ; Nerve Tissue Proteins
Chemical Substances	Amyloid beta-Peptides ; DNA-Binding Proteins ; TMEM106B protein, human ; Membrane Proteins ; Nerve Tissue Proteins
Language	English
Publishing date	2023-05-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-221094
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Article ; Online: Old age amyotrophic lateral sclerosis and limbic TDP-43 pathology.

Murakami, Aya / Koga, Shunsuke / Sekiya, Hiroaki / Oskarsson, Björn / Boylan, Kevin / Petrucelli, Leonard / Josephs, Keith A / Dickson, Dennis W

Brain pathology (Zurich, Switzerland)

2022 Volume 32, Issue 6, Page(s) e13100

Abstract: This study aimed to assess and compare the burden of transactive response DNA-binding protein of 43 kDa (TDP-43) pathology and clinical features of amyotrophic lateral sclerosis (ALS) in three age groups. All cases were from the Mayo Clinic brain bank ... ...

Abstract	This study aimed to assess and compare the burden of transactive response DNA-binding protein of 43 kDa (TDP-43) pathology and clinical features of amyotrophic lateral sclerosis (ALS) in three age groups. All cases were from the Mayo Clinic brain bank for neurodegenerative disorders and most were followed longitudinally in the ALS Clinic. Cases with moderate-to-severe Alzheimer's disease neuropathological change were excluded. The 55 cases included in the study were divided into three groups by age at death: 75 years or older (old-ALS, n = 8), 64-74 years (middle-ALS, n = 23), and 63 years or younger (young-ALS, n = 24). Clinical features, including disease duration, initial symptoms, and ALS Cognitive Behavior Score (ALS-CBS), were summarized. Sections of paraffin-embedded tissue from the motor cortex, basal forebrain, medial temporal lobe, and middle frontal gyrus were processed for phospho-TDP-43 immunohistochemistry. The burden of TDP-43 pathology was analyzed using digital image analysis. The TDP-43 burden in the limbic system (i.e., amygdala, dentate gyrus and CA1 sector of the hippocampus, subiculum, and entorhinal cortex) was greater in old-ALS than in young-ALS and middle-ALS. TDP-43 burden in the middle frontal gyrus was sparse and did not differ between the three groups. The average of ALS-CBS was not different between the three groups. The present study shows that the amygdala and hippocampus are vulnerable to TDP-43 pathology in older patients with ALS. We discuss the evidence for and against this pathology being related to concurrent limbic-predominant, age-related TDP-43 encephalopathy neuropathologic change.
MeSH term(s)	Humans ; Aged ; Amyotrophic Lateral Sclerosis/pathology ; DNA-Binding Proteins/metabolism ; Alzheimer Disease/pathology ; Brain/pathology ; Hippocampus/pathology ; TDP-43 Proteinopathies/metabolism
Chemical Substances	DNA-Binding Proteins
Language	English
Publishing date	2022-06-17
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.13100
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Article ; Online: Histologic tau lesions and magnetic resonance imaging biomarkers differ across two progressive supranuclear palsy variants.

Orlandi, Francesca / Carlos, Arenn F / Ali, Farwa / Clark, Heather M / Duffy, Joseph R / Utianski, Rene L / Botha, Hugo / Machulda, Mary M / Stephens, Yehkyoung C / Schwarz, Christopher G / Senjem, Matthew L / Jack, Clifford R / Agosta, Federica / Filippi, Massimo / Dickson, Dennis W / Josephs, Keith A / Whitwell, Jennifer L

Brain communications

2024 Volume 6, Issue 2, Page(s) fcae113

Abstract: Progressive supranuclear palsy is a neurodegenerative disease characterized by the deposition of four-repeat tau in neuronal and glial lesions in the brainstem, cerebellar, subcortical and cortical brain regions. There are varying clinical presentations ... ...

Abstract	Progressive supranuclear palsy is a neurodegenerative disease characterized by the deposition of four-repeat tau in neuronal and glial lesions in the brainstem, cerebellar, subcortical and cortical brain regions. There are varying clinical presentations of progressive supranuclear palsy with different neuroimaging signatures, presumed to be due to different topographical distributions and burden of tau. The classic Richardson syndrome presentation is considered a subcortical variant, whilst progressive supranuclear palsy with predominant speech and language impairment is considered a cortical variant, although the pathological underpinnings of these variants are unclear. In this case-control study, we aimed to determine whether patterns of regional tau pathology differed between these variants and whether tau burden correlated with neuroimaging. Thirty-three neuropathologically confirmed progressive supranuclear palsy patients with either the Richardson syndrome (
Language	English
Publishing date	2024-04-05
Publishing country	England
Document type	Journal Article
ISSN	2632-1297
ISSN (online)	2632-1297
DOI	10.1093/braincomms/fcae113
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Article ; Online: Longitudinal characterization of patients with progressive apraxia of speech without clearly predominant phonetic or prosodic speech features.

Utianski, Rene L / Meade, Gabriela / Duffy, Joseph R / Clark, Heather M / Botha, Hugo / Machulda, Mary M / Dickson, Dennis W / Whitwell, Jennifer L / Josephs, Keith A

Brain and language

2023 Volume 245, Page(s) 105314

Abstract: Most recent studies of progressive apraxia of speech (PAOS) have focused on patients with phonetic or prosodic predominant PAOS to understand the implications of the presenting clinical phenotype. Patients without a clearly predominating speech quality, ... ...

Abstract	Most recent studies of progressive apraxia of speech (PAOS) have focused on patients with phonetic or prosodic predominant PAOS to understand the implications of the presenting clinical phenotype. Patients without a clearly predominating speech quality, or mixed AOS, have been excluded. Given the implications for disease progression, it is important to understand these patients early in the disease course to inform appropriate education and prognostication. The aim of this study was to describe a cohort of ten patients with initially mixed PAOS and how their clinical course evolves. Four patients were rated prosodic predominant later on (mild AOS at first visit); five were later designated phonetic (four with more than mild AOS at first visit); one was judged mixed at all visits. The study suggests patients without a clear predominance of speech featuresshould still be included in PAOS studies and thought of on the continuum of the disease spectrum.
Language	English
Publishing date	2023-08-20
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	7448-2
ISSN	1090-2155 ; 0093-934X
ISSN (online)	1090-2155
ISSN	0093-934X
DOI	10.1016/j.bandl.2023.105314
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Article ; Online: Amyloid and Tau PET Positivity in Progressive Agrammatic Aphasia and Apraxia of Speech.

Tetzloff, Katerina A / Duffy, Joseph R / Clark, Heather M / Pham, Nha Trang Thu / Machulda, Mary M / Botha, Hugo / Jack, Clifford R / Dickson, Dennis W / Lowe, Val J / Josephs, Keith A / Whitwell, Jennifer L / Utianski, Rene L

Journal of Alzheimer's disease : JAD

2023 Volume 96, Issue 4, Page(s) 1759–1765

Abstract: Background: The agrammatic variant of primary progressive aphasia (PAA), primary progressive apraxia of speech (PPAOS), or a combination of both (AOS-PAA) are neurodegenerative disorders characterized by speech-language impairments and together compose ... ...

Abstract	Background: The agrammatic variant of primary progressive aphasia (PAA), primary progressive apraxia of speech (PPAOS), or a combination of both (AOS-PAA) are neurodegenerative disorders characterized by speech-language impairments and together compose the AOS-PAA spectrum disorders. These patients typically have an underlying 4-repeat tauopathy, although they sometimes show evidence of amyloid-β and tau deposition on PET, suggesting Alzheimer's disease (AD). Given the growing number of pharmacologic treatment options for AD, it is important to better understand the incidence of AD pathology in these patients. Objective: This study aimed to evaluate the frequency of amyloid-β and tau positivity in AOS-PAA spectrum disorders. Sixty-five patients with AOS-PAA underwent a clinical speech-language battery and PiB PET and flortaucipir PET imaging. Methods: Global PiB PET standardized uptake value ratios (SUVRs) and flortaucipir PET SUVRs from the temporal meta region of interest were compared between patient groups. For 19 patients who had died and undergone autopsy, their PET and pathology findings were also compared. Results: The results showed that although roughly half of the patients are positive for at least one biomarker, their clinical symptoms and biomarker status were not related, suggesting that AD is not the primary cause of their neurodegeneration. All but one patient in the autopsy subset had a Braak stage of IV or less, despite four being positive on tau PET imaging. Conclusions: Inclusion criteria for clinical trials should specify clinical presentation or adjust the evaluation of such treatments to be specific to disease diagnosis beyond the presence of certain imaging biomarkers.
MeSH term(s)	Humans ; Alzheimer Disease/diagnostic imaging ; Alzheimer Disease/pathology ; Amyloid/metabolism ; Amyloid beta-Peptides/metabolism ; Aphasia ; Apraxias ; Biomarkers ; Brain/pathology ; Positron-Emission Tomography/methods ; Speech ; tau Proteins/metabolism
Chemical Substances	Amyloid ; Amyloid beta-Peptides ; Biomarkers ; tau Proteins ; MAPT protein, human ; APP protein, human
Language	English
Publishing date	2023-11-24
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1440127-7
ISSN	1875-8908 ; 1387-2877
ISSN (online)	1875-8908
ISSN	1387-2877
DOI	10.3233/JAD-230912
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Article: The carotenemia of hypothyroidism.

JOSEPHS, H W

The Journal of pediatrics

2003 Volume 41, Issue 6, Page(s) 784–791

MeSH term(s)	Carotenoids/blood ; Humans ; Hypothyroidism ; Pigmentation Disorders
Chemical Substances	Carotenoids (36-88-4)
Language	English
Publishing date	2003-04-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	3102-1
ISSN	1097-6833 ; 0022-3476
ISSN (online)	1097-6833
ISSN	0022-3476
DOI	10.1016/s0022-3476(52)80298-7
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