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Article ; Online: Loss of putative GABAergic neurons in the ventrolateral medulla in multiple system atrophy.

Schmeichel, Ann M / Coon, Elizabeth A / Parisi, Joseph E / Singer, Wolfgang / Low, Phillip A / Benarroch, Eduardo E

2022 Volume 44, Issue 9

Abstract: Study objectives: Multiple system atrophy (MSA) is associated with disturbances in cardiovascular, sleep and respiratory control. The lateral paragigantocellular nucleus (LPGi) in the ventrolateral medulla (VLM) contains GABAergic neurons that ... ...

Abstract	Study objectives: Multiple system atrophy (MSA) is associated with disturbances in cardiovascular, sleep and respiratory control. The lateral paragigantocellular nucleus (LPGi) in the ventrolateral medulla (VLM) contains GABAergic neurons that participate in control of rapid eye movement (REM) sleep and cardiovagal responses. We sought to determine whether there was loss of putative GABAergic neurons in the LPGi and adjacent regions in MSA. Methods: Sections of the medulla were processed for GAD65/67 immunoreactivity in eight subjects with clinical and neuropathological diagnosis of MSA and in six control subjects. These putative GABAergic LPGi neurons were mapped based on their relationship to adjacent monoaminergic VLM groups. Results: There were markedly decreased numbers of GAD-immunoreactive neurons in the LPGi and adjacent VLM regions in MSA. Conclusions: There is loss of GABAergic neurons in the VLM, including the LPGi in patients with MSA. Whereas these findings provide a possible mechanistic substrate, given the few cases included, further studies are necessary to determine whether they contribute to REM sleep-related cardiovagal and possibly respiratory dysregulation in MSA.
MeSH term(s)	GABAergic Neurons ; Humans ; Medulla Oblongata ; Multiple System Atrophy ; Sleep, REM
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	424441-2
ISSN	1550-9109 ; 0161-8105
ISSN (online)	1550-9109
ISSN	0161-8105
DOI	10.1093/sleep/zsab074
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Article ; Online: 2015 Award Recipients-Bette Kay Kleinschmidt-DeMasters, MD and John Q. Trojanowski, MD, PhD.

Parisi, Joseph E / Nelson, Peter T

Journal of neuropathology and experimental neurology

2015 Volume 74, Issue 10, Page(s) 1036–1038

MeSH term(s)	Awards and Prizes ; History, 20th Century ; History, 21st Century ; Neurology/history ; United States
Language	English
Publishing date	2015-10
Publishing country	England
Document type	Biography ; Historical Article ; Journal Article
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1097/NEN.0000000000000243
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Article ; Online: A Woman in Her 60s With Chronic Meningitis.

Pichler, Michael R / Parisi, Joseph E / Klaas, James P

JAMA neurology

2017 Volume 74, Issue 3, Page(s) 348–352

Abstract: A renal transplant recipient in her 60s presented with a history of chronic headaches and progressive encephalopathy. Serial cerebrospinal fluid examinations were consistent with chronic lymphocytic meningitis, but no definitive cause was identified. ... ...

Abstract	A renal transplant recipient in her 60s presented with a history of chronic headaches and progressive encephalopathy. Serial cerebrospinal fluid examinations were consistent with chronic lymphocytic meningitis, but no definitive cause was identified. Imaging studies showed the development of an enhancing suprasellar mass lesion and hydrocephalus. Symptoms progressed despite empiric antimicrobial therapy, and the patient died after an acute large-volume subarachnoid hemorrhage. A complete autopsy was performed. The differential diagnosis, pathologic findings, and diagnosis are discussed.
MeSH term(s)	Aspergillosis/complications ; Aspergillosis/etiology ; Aspergillus/physiology ; Chronic Disease ; Female ; Humans ; Kidney Transplantation/adverse effects ; Meningitis/diagnostic imaging ; Meningitis/etiology ; Middle Aged ; Postoperative Complications/physiopathology
Language	English
Publishing date	2017-03-01
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2016.2388
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Article ; Online: Spectrum of sublytic astrocytopathy in neuromyelitis optica.

Guo, Yong / Lennon, Vanda A / Parisi, Joseph E / Popescu, Bogdan / Vasquez, Christina / Pittock, Sean J / Howe, Charles L / Lucchinetti, Claudia F

Brain : a journal of neurology

2021 Volume 145, Issue 4, Page(s) 1379–1390

Abstract: Neuromyelitis optica is an autoimmune inflammatory disorder targeting aquaporin-4 water channels in CNS astrocytes. Histopathological descriptions of astrocytic lesions reported in neuromyelitis optica so far have emphasized a characteristic loss of ... ...

Abstract	Neuromyelitis optica is an autoimmune inflammatory disorder targeting aquaporin-4 water channels in CNS astrocytes. Histopathological descriptions of astrocytic lesions reported in neuromyelitis optica so far have emphasized a characteristic loss of aquaporin-4, with deposition of IgG and complement and lysis of astrocytes, but sublytic reactions have been underappreciated. We performed a multi-modality study of 23 neuromyelitis optica autopsy cases (clinically and/or pathologically confirmed; 337 tissue blocks). By evaluating astrocytic morphology, immunohistochemistry and AQP4 RNA transcripts, and their associations with demyelinating activity, we documented a spectrum of astrocytopathy in addition to complement deposition, microglial reaction, granulocyte infiltration and regenerating activity. Within advanced demyelinating lesions, and in periplaque areas, there was remarkable hypertrophic astrogliosis, more subtle than astrocytic lysis. A degenerative component was suggested by 'dystrophic' morphology, cytoplasmic vacuolation, Rosenthal fibres and associated stress protein markers. The abundance of AQP4 mRNA transcripts in sublytic reactive astrocytes devoid of aquaporin-4 protein supported in vivo restoration following IgG-induced aquaporin-4 endocytosis/degradation. Astrocytic alterations extending beyond demyelinating lesions speak to astrocytopathy being an early and primary event in the evolving neuromyelitis optica lesion. Focal astrocytopathy observed without aquaporin-4 loss or lytic complement component deposition verifies that astrocytic reactions in neuromyelitis optica are not solely dependent on IgG-mediated aquaporin-4 loss or lysis by complement or by IgG-dependent leucocyte mediators. We conclude that neuromyelitis optica reflects a global astrocytopathy, initiated by binding of IgG to aquaporin-4 and not simply definable by demyelination and astrocytic lysis. The spectrum of astrocytic morphological changes in neuromyelitis optica attests to the complexity of factors influencing the range of astrocytic physiological responses to a targeted attack by aquaporin-4-specific IgG. Sublytic astrocytic reactions are no doubt an important determinant of the lesion's evolution and potential for repair. Pharmacological manipulation of the astrocytic stress response may offer new avenues for therapeutic intervention.
MeSH term(s)	Aquaporin 4 ; Astrocytes/metabolism ; Humans ; Immunoglobulin G/metabolism ; Neuromyelitis Optica/metabolism
Chemical Substances	Aquaporin 4 ; Immunoglobulin G
Language	English
Publishing date	2021-10-30
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80072-7
ISSN	1460-2156 ; 0006-8950
ISSN (online)	1460-2156
ISSN	0006-8950
DOI	10.1093/brain/awab394
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Article ; Online: Intractable Epilepsy and Progressive Cognitive Decline in a Young Man.

Cohen, Alexander L / Jones, Lyell K / Parisi, Joseph E / Klaas, James P

JAMA neurology

2017 Volume 74, Issue 6, Page(s) 737–740

Abstract: A young man with normal neurodevelopment presented with 3 years of medically refractory, progressive epilepsy and myoclonus. Initial examination included neuroimaging, electroencephalography, and biochemical analyses, all of which were unremarkable ... ...

Abstract	A young man with normal neurodevelopment presented with 3 years of medically refractory, progressive epilepsy and myoclonus. Initial examination included neuroimaging, electroencephalography, and biochemical analyses, all of which were unremarkable except for mildly enlarged ventricles. Over the following year, the patient experienced rapid cognitive decline with new-onset recurrent visual hallucinations and progressive lethargy. Results of subsequent electroencephalography and brain imaging were unchanged, and a fluorodeoxyglucose F 18 positron emission tomographic scan was normal.
MeSH term(s)	Adult ; Cognition Disorders/diagnosis ; Cognition Disorders/etiology ; Disease Progression ; Drug Resistant Epilepsy/complications ; Drug Resistant Epilepsy/diagnosis ; Humans ; Lafora Disease/complications ; Lafora Disease/diagnosis ; Male ; Young Adult
Language	English
Publishing date	2017-04-06
Publishing country	United States
Document type	Journal Article
ZDB-ID	2702023-X
ISSN	2168-6157 ; 2168-6149
ISSN (online)	2168-6157
ISSN	2168-6149
DOI	10.1001/jamaneurol.2016.3195
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Article ; Online: Exploring Gene Expression Profiles in Primary Central Nervous System Vasculitis.

Salvarani, Carlo / Paludo, Jonas / Hunder, Gene G / Ansell, Stephen M / Giannini, Caterina / Parisi, Joseph E / Huston, John / Koster, Matthew J / Warrington, Kenneth J / Croci, Stefania / Brown, Robert D

Annals of neurology

2022 Volume 93, Issue 1, Page(s) 120–130

Abstract: Objective: This study was undertaken to explore the gene expression profile of primary central nervous system vasculitis (PCNSV).: Methods: Brain specimens of 4 patients with granulomatous vasculitis (GV), 5 with lymphocytic vasculitis (LV), 4 with ... ...

Abstract	Objective: This study was undertaken to explore the gene expression profile of primary central nervous system vasculitis (PCNSV). Methods: Brain specimens of 4 patients with granulomatous vasculitis (GV), 5 with lymphocytic vasculitis (LV), 4 with amyloid β-related angiitis (ABRA), and 4 normal controls were studied. RNA-sequencing was performed using the Illumina Hiseq-4,000 platform and the Illumina TruSeq Total-RNA library. Student t test and false discovery rate tests were performed for each of the differentially expressed transcripts. Ingenuity Pathway Analysis was used for the pathway expression analysis. CIBERSORT was used to estimate the abundances of different immune cell subsets in the tissues based on gene expression data. Results: Transcripts differentially expressed between PCNSV and normal brain indicated that endosomal, mitochondrial, and ribosome dysfunction, alterations in protein synthesis, and noncoding RNAs might be involved in PCNSV. Pathway analysis revealed the activation of dendritic cell maturation and antigen processing as well as neuroinflammation in PCNSV versus normal brain, whereas oxidative phosphorylation was inhibited. CIBERSORT estimation of immune cell subsets suggested that activated NK cells, M1 macrophages, memory B cells, and follicular helper T cells were likely to be more prevalent in PCNSV samples. Naïve CD4 T cells and monocytes were mainly estimated to be present in GV and ABRA. Plasma cell and γδ T-cell signatures were mainly found in LV and normal brain. GV showed higher levels of genes associated with macrophage activities and T cells. ABRA showed higher levels of long noncoding RNAs and miR-616. LV showed higher levels of genes encoding immunoglobulins. Interpretation: RNA sequencing confirmed PCNSV heterogeneity. ANN NEUROL 2023;93:120-130.
MeSH term(s)	Humans ; Amyloid beta-Peptides/metabolism ; Transcriptome ; Magnetic Resonance Imaging ; Vasculitis, Central Nervous System/genetics ; RNA ; MicroRNAs
Chemical Substances	Amyloid beta-Peptides ; RNA (63231-63-0) ; MIRN616 microRNA, human ; MicroRNAs
Language	English
Publishing date	2022-11-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	80362-5
ISSN	1531-8249 ; 0364-5134
ISSN (online)	1531-8249
ISSN	0364-5134
DOI	10.1002/ana.26537
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Zs.A 1370: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: Chronic traumatic encephalopathy in an epilepsy surgery cohort: Clinical and pathologic findings.

Jones, Amy L / Britton, Jeffrey W / Blessing, Melissa M / Parisi, Joseph E / Cascino, Gregory D

Neurology

2018 Volume 90, Issue 6, Page(s) e474–e478

Abstract: Objective: To determine the occurrence of chronic traumatic encephalopathy (CTE) in young adult patients undergoing epilepsy surgery.: Methods: Ten patients who underwent epilepsy surgery were randomly selected for this retrospective study. The ... ...

Abstract	Objective: To determine the occurrence of chronic traumatic encephalopathy (CTE) in young adult patients undergoing epilepsy surgery. Methods: Ten patients who underwent epilepsy surgery were randomly selected for this retrospective study. The patients were 18-45 years of age, had preoperative neuropsychological evaluation, and had 1 year postoperative follow-up. Microscopic sections from resections were evaluated for the presence of CTE with standard stains and antibodies to tau (clone AT8). Results: The median age at resection was 32.5 years (range 23-43) and the median duration of seizures was 23.5 years (range 3-28). Eight had a history of head injury. Preoperative neuropsychological testing showed mild to moderate cognitive impairment in 8 patients (80%). Pathologic examination in one patient showed focal sparse tau-immunoreactive lesions along descending rami and cortical gyral depths of the resected frontal lobe. Nine patients had no evidence of CTE. All focal cortical resections showed variable subpial and subcortical gliosis commonly identified in patients with chronic seizure disorders. Conclusions: The present small retrospective observational study suggests that CTE may occur, but appears uncommon, in young adult patients undergoing surgical treatment for drug-resistant focal epilepsy. The significance of these findings requires further investigation to define the relative importance of tau accumulation in younger adult patients with drug-resistant focal epilepsy and cognitive decline.
MeSH term(s)	Adult ; Cerebral Cortex/metabolism ; Cerebral Cortex/pathology ; Chronic Traumatic Encephalopathy/etiology ; Chronic Traumatic Encephalopathy/pathology ; Electroencephalography ; Epilepsy/complications ; Epilepsy/surgery ; Female ; France ; Humans ; Male ; Middle Aged ; Pilot Projects ; Postoperative Complications/pathology ; Retrospective Studies ; Young Adult ; tau Proteins/metabolism
Chemical Substances	tau Proteins
Language	English
Publishing date	2018-01-10
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000004927
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Article ; Online: Demographics and clinical characteristics of episodic hypothermia in multiple sclerosis.

Toledano, Michel / Weinshenker, Brian G / Kaufmann, Timothy J / Parisi, Joseph E / Paz Soldán, M Mateo

Multiple sclerosis (Houndmills, Basingstoke, England)

2018 Volume 25, Issue 5, Page(s) 709–714

Abstract: Background: Episodic hypothermia (EH) can occur in multiple sclerosis (MS). The putative mechanism is impairment of thermoregulation due to a presumed demyelinating hypothalamic lesion.: Objective: To describe a cohort of patients with MS, who ... ...

Abstract	Background: Episodic hypothermia (EH) can occur in multiple sclerosis (MS). The putative mechanism is impairment of thermoregulation due to a presumed demyelinating hypothalamic lesion. Objective: To describe a cohort of patients with MS, who developed EH. Methods: Patients were identified through review of the Mayo Clinic electronic medical record (1996 to July 2015). Search terms were [multiple sclerosis] or [MS] within the diagnoses field and [hypothermia] within any field. We reviewed records for accuracy of diagnoses and abstracted relevant data. Magnetic resonance imaging (MRI) was reviewed for presence of hypothalamic lesions. Results: Of 156 patients, 34 had concurrent MS and hypothermia. Thirty-two (94%) had progressive disease at EH onset. Median MS duration was 19.9 years, and median expanded disability status scale (EDSS) was 8.0. Most patients presented with alterations in consciousness. Infection was suspected as the precipitating factor in 19 (56%), but clinically/laboratory supported in only 9 (28%). MRI lesions were evident within the hypothalamus in only 4 (14%). Conclusion: EH occurs predominantly in patients with advanced secondary progressive MS. The major manifestation is altered consciousness. Infection is often suspected as causal, but infrequently confirmed. Although commonly implicated, hypothalamic lesions were rarely evident on MRI and were absent in two post-mortem evaluations.
MeSH term(s)	Adult ; Brain/pathology ; Cohort Studies ; Demography/methods ; Disability Evaluation ; Disease Progression ; Female ; Humans ; Hypothermia/diagnosis ; Hypothermia/pathology ; Magnetic Resonance Imaging/methods ; Male ; Middle Aged ; Multiple Sclerosis/diagnosis ; Multiple Sclerosis/pathology
Language	English
Publishing date	2018-03-23
Publishing country	England
Document type	Journal Article
ZDB-ID	1290669-4
ISSN	1477-0970 ; 1352-4585
ISSN (online)	1477-0970
ISSN	1352-4585
DOI	10.1177/1352458518767045
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Article ; Online: Coprophagia in neurologic disorders.

Josephs, Keith A / Whitwell, Jennifer L / Parisi, Joseph E / Lapid, Maria I

Journal of neurology

2016 Volume 263, Issue 5, Page(s) 1008–1014

Abstract: We report on the unusual behavior of coprophagia (eating one's own feces) in neurologic disorders. The Mayo Clinic Health Sciences-computerized clinical database was queried for all patients evaluated at our institution between 1995 and 2015 in which ... ...

Abstract	We report on the unusual behavior of coprophagia (eating one's own feces) in neurologic disorders. The Mayo Clinic Health Sciences-computerized clinical database was queried for all patients evaluated at our institution between 1995 and 2015 in which coprophagia was documented in the medical records. Twenty-six patients were identified of which 17 had coprophagia. Of the 17 patients, five were excluded due to age at onset less than 10 years, leaving 12 adult patients for this study. The median age at onset of coprophagia in the 12 patients was 55 years (range 20-88 years), and half were female. Additional behaviors were common including scatolia (fecal smearing), hypersexuality, aggression, and pica (eating objects of any kind). Coprophagia was associated with neurodegenerative dementia in six patients, developmental delay in two, and one each with seizures, steroid psychosis, frontal lobe tumor, and schizoaffective disorder. Brain imaging in the six patients with dementia showed moderate-to-severe medial temporal lobe atrophy, as well as mild frontal lobe atrophy. Autopsy examination was performed in one patient and revealed frontotemporal lobar degeneration pathology. Many different behavioral and pharmacologic therapies were implemented, yet only haloperidol was associated with discontinuation of the behavior. Coprophagia is associated with different neurologic disorders, particularly neurodegenerative dementias. The behavior may be related to medial temporal lobe atrophy, similar to the Klüver-Bucy syndrome. Haloperidol appears to be effective in treating the behavior, at least in some patients.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Brain/diagnostic imaging ; Female ; Human Coprophagia/complications ; Human Coprophagia/diagnostic imaging ; Human Coprophagia/epidemiology ; Human Coprophagia/therapy ; Humans ; Male ; Middle Aged ; Nervous System Diseases/complications ; Nervous System Diseases/diagnostic imaging ; Nervous System Diseases/epidemiology ; Nervous System Diseases/therapy ; Young Adult
Language	English
Publishing date	2016-05
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/s00415-016-8096-1
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Article ; Online: TDP-43-associated atrophy in brains with and without frontotemporal lobar degeneration.

Buciuc, Marina / Martin, Peter R / Tosakulwong, Nirubol / Murray, Melissa E / Petrucelli, Leonard / Senjem, Matthew L / Spychalla, Anthony J / Knopman, David S / Boeve, Bradley F / Petersen, Ronald C / Parisi, Joseph E / Reichard, R Ross / Dickson, Dennis W / Jack, Clifford R / Whitwell, Jennifer L / Josephs, Keith A

NeuroImage. Clinical

2022 Volume 34, Page(s) 102954

Abstract: Transactive response DNA-binding protein of ∼43 kDa (TDP-43), a primary pathologic substrate in tau-negative frontotemporal lobar degeneration (FTLD), is also often found in the brains of elderly individuals without FTLD and is a key player in the ... ...

Abstract	Transactive response DNA-binding protein of ∼43 kDa (TDP-43), a primary pathologic substrate in tau-negative frontotemporal lobar degeneration (FTLD), is also often found in the brains of elderly individuals without FTLD and is a key player in the process of neurodegeneration in brains with and without FTLD. It is unknown how rates and trajectories of TDP-43-associated brain atrophy compare between these two groups. Additionally, non-FTLD TDP-43 inclusions are not homogeneous and can be divided into two morphologic types: type-α and neurofibrillary tangle-associated type-β. Therefore, we explored whether neurodegeneration also varies due to the morphologic type. In this longitudinal retrospective study of 293 patients with 843 MRI scans spanning over ∼10 years, we used a Bayesian hierarchical linear model to quantify similarities and differences between the non-FTLD TDP-43 (type-α/type-β) and FTLD-TDP (n = 68) in both regional volume at various timepoints before death and annualized rate of atrophy. Since Alzheimer's disease (AD) is a frequent co-pathology in non-FTLD TDP-43, we further divided types α/β based on presence/absence of intermediate-high likelihood AD: AD-TDP type-β (n = 90), AD-TDP type-α (n = 104), and Pure-TDP (n = 31, all type-α). FTLD-TDP was associated with faster atrophy rates in the inferior temporal lobe and temporal pole compared to all non-FTLD TDP-43 groups. The atrophy rate in the frontal lobe was modulated by age with younger FTLD-TDP having the fastest rates. Older FTLD-TDP showed a limbic predominant pattern of neurodegeneration. AD-TDP type-α showed faster rates of hippocampal atrophy and smaller volumes of amygdala, temporal pole, and inferior temporal lobe compared to AD-TDP type-β. Pure-TDP was associated with slowest rates and less atrophy in all brain regions. The results suggest that there are differences and similarities in longitudinal brain volume loss between FTLD-TDP and non-FTLD TDP-43. Within FTLD-TDP age plays a role in which brain regions are the most affected. Additionally, brain atrophy regional rates also vary by non-FTLD TDP-43 type.
MeSH term(s)	Aged ; Alzheimer Disease/pathology ; Atrophy/pathology ; Bayes Theorem ; Brain/pathology ; DNA-Binding Proteins/metabolism ; Frontotemporal Dementia/pathology ; Frontotemporal Lobar Degeneration/diagnostic imaging ; Frontotemporal Lobar Degeneration/pathology ; Humans ; Retrospective Studies
Chemical Substances	DNA-Binding Proteins ; TARDBP protein, human
Language	English
Publishing date	2022-02-04
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2701571-3
ISSN	2213-1582 ; 2213-1582
ISSN (online)	2213-1582
ISSN	2213-1582
DOI	10.1016/j.nicl.2022.102954
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