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Article ; Online: Fatal Granulomatous Amebic Encephalitis in a Heart Transplant Patient: Clinical, Radiographic, and Autopsy Findings.

Harrison, William T / Lecky, Bruce / Hulette, Christine M

Journal of neuropathology and experimental neurology

2018 Volume 77, Issue 11, Page(s) 1001–1004

Abstract: Granulomatous amebic encephalitis is a rare necrotizing infection of the CNS that occurs most commonly in immunocompromised individuals and is usually fatal. It is difficult to diagnose as the clinical symptoms and radiographic findings are often ... ...

Abstract	Granulomatous amebic encephalitis is a rare necrotizing infection of the CNS that occurs most commonly in immunocompromised individuals and is usually fatal. It is difficult to diagnose as the clinical symptoms and radiographic findings are often mistaken for other bacterial, viral, fungal, or protozoan infections. Herein, we present the case of a 69-year-old heart transplant recipient who suffered fulminant neurological decline ∼5 months after transplant. Extensive radiographic and laboratory testing did not provide a definite anatomic diagnosis and, despite aggressive clinical treatment, he died. An autopsy examination demonstrated numerous brain abscesses which contained amebic trophozoites and cysts. An indirect immunofluorescence assay performed at the Centers for Disease Control confirmed the presence of Acanthamoeba species. To the best of our knowledge, only 13 other cases of Acanthamoeba amebic encephalitis have been reported in patients who have received solid organ transplants and this is the second case reported in a heart transplant recipient. This case emphasizes that amebic encephalitis should be in the differential diagnosis for immunocompromised patients with new brain lesions found on radiographic imaging.
MeSH term(s)	Acanthamoeba/pathogenicity ; Aged ; Autopsy ; Central Nervous System Protozoal Infections/diagnostic imaging ; Central Nervous System Protozoal Infections/etiology ; Fatal Outcome ; Heart Transplantation/adverse effects ; Humans ; Infectious Encephalitis/diagnostic imaging ; Infectious Encephalitis/etiology ; Magnetic Resonance Imaging ; Male
Language	English
Publishing date	2018-10-07
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/nly089
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Article: Brain banking in the United States.

Hulette, Christine M

Journal of neuropathology and experimental neurology

2003 Volume 62, Issue 7, Page(s) 715–722

Abstract: Many of us who conduct research based on disorders that uniquely affect the human nervous system are involved directly or indirectly with brain banks. Brain banking is by its very nature a multi-disciplinary endeavor that requires close collaboration ... ...

Abstract	Many of us who conduct research based on disorders that uniquely affect the human nervous system are involved directly or indirectly with brain banks. Brain banking is by its very nature a multi-disciplinary endeavor that requires close collaboration with our colleagues in clinical departments and also with the families and patients who are donors of brain tissue. These brain tissues will ultimately be used for many types of basic science investigations. Thus, many brain banks are as unique as the basic research programs that they serve. However, there are some commonalities in the field of brain banking. This paper represents a broad overview of brain banking and the issues that are common to all brain banks. Legal and ethical concerns regarding confidentiality of donor records and donor recruitment procedures, as well as safety precautions for technical staff, tissue banking methods and disbursement will be discussed. Finally, issues surrounding financial support for brain banks will be considered.
MeSH term(s)	Brain/pathology ; Education, Medical, Graduate/trends ; Humans ; Interdisciplinary Communication ; Neurology/trends ; Occupational Health ; Pathology/trends ; Tissue Banks/trends ; Tissue Donors/ethics ; United States
Language	English
Publishing date	2003-05-16
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1093/jnen/62.7.715
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Article ; Online: Atypical lymphocytic angiitis of the optic nerve and central nervous system.

Lad, Eleonora M / Hulette, Christine M / Proia, Alan D

JAMA ophthalmology

2014 Volume 132, Issue 11, Page(s) 1373–1375

MeSH term(s)	B-Lymphocytes/metabolism ; B-Lymphocytes/pathology ; Biomarkers/metabolism ; Blindness/diagnosis ; Fatal Outcome ; Fibrosis ; Humans ; Male ; Optic Nerve Diseases/diagnosis ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; Vasculitis, Central Nervous System/diagnosis
Chemical Substances	Biomarkers
Language	English
Publishing date	2014-11
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2701705-9
ISSN	2168-6173 ; 2168-6165
ISSN (online)	2168-6173
ISSN	2168-6165
DOI	10.1001/jamaophthalmol.2014.2786
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Article: Neuropathology of Alzheimer's disease.

Mott, Ryan T / Hulette, Christine M

Neuroimaging clinics of North America

2005 Volume 15, Issue 4, Page(s) 755–65, ix

Abstract: In 1907, Alois Alzheimer described the presence of plaques and neurofibrillary tangles in a demented patient. Currently, Alzheimer's disease is known to be the most common cause of dementia in elderly patients. In this article, we summarize the most ... ...

Abstract	In 1907, Alois Alzheimer described the presence of plaques and neurofibrillary tangles in a demented patient. Currently, Alzheimer's disease is known to be the most common cause of dementia in elderly patients. In this article, we summarize the most important neuropathologic features of Alzheimer's disease, including amyloid plaques, neurofibrillary tangles, neuronal loss, synaptic depletion, cerebral amyloid angiopathy, Hirano bodies, and granulovacuolar degeneration. We also review the history and application of Alzheimer's disease diagnostic criteria.
MeSH term(s)	Alzheimer Disease/pathology ; Brain/pathology ; Humans
Language	English
Publishing date	2005-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1314594-0
ISSN	1052-5149
ISSN	1052-5149
DOI	10.1016/j.nic.2005.09.003
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Article ; Online: Coronary artery disease is associated with Alzheimer disease neuropathology in APOE4 carriers.

Hulette, Christine M / Welsh-Bohmer, Kathleen

Neurology

2007 Volume 68, Issue 6, Page(s) 471; author reply 471

MeSH term(s)	Aged, 80 and over ; Alleles ; Alzheimer Disease/complications ; Alzheimer Disease/genetics ; Alzheimer Disease/pathology ; Aortic Diseases/complications ; Aortic Diseases/genetics ; Apolipoprotein E4/genetics ; Atherosclerosis/complications ; Atherosclerosis/genetics ; Brain/pathology ; Cardiomegaly/complications ; Cardiomegaly/genetics ; Cardiomegaly/pathology ; Comorbidity ; Coronary Disease/complications ; Coronary Disease/genetics ; Female ; Genetic Predisposition to Disease ; Genotype ; Heart Ventricles/pathology ; Humans ; Male ; Neurofibrillary Tangles ; Organ Size ; Plaque, Amyloid ; Severity of Illness Index
Chemical Substances	Apolipoprotein E4
Language	English
Publishing date	2007-02-06
Publishing country	United States
Document type	Comment ; Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/01.wnl.0000256286.78188.dd
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Article: RB1CC1 insufficiency causes neuronal atrophy through mTOR signaling alteration and involved in the pathology of Alzheimer's diseases.

Chano, Tokuhiro / Okabe, Hidetoshi / Hulette, Christine M

Brain research

2007 Volume 1168, Page(s) 97–105

Abstract: RB1-inducible Coiled-Coil 1 (RB1CC1) has been shown to be a novel tumor suppressor regulating RB1 expression. Neuronal abundance of RB1CC1 is reported to contribute to the non-proliferating enlarged cell phenotype through the maintenance of RB1 and mTOR. ...

Abstract	RB1-inducible Coiled-Coil 1 (RB1CC1) has been shown to be a novel tumor suppressor regulating RB1 expression. Neuronal abundance of RB1CC1 is reported to contribute to the non-proliferating enlarged cell phenotype through the maintenance of RB1 and mTOR. To clarify whether RB1CC1 insufficiency is involved in neuronal atrophy and Alzheimer's pathology, we investigated modifications of RB1CC1 as a possible cause of atrophy or death through the disturbance of mTOR signaling in Neuro-2a neuroblastoma cells. We also evaluated the correlation between RB1CC1 and mTOR signaling in a series of Alzheimer's brain tissues. Though RB1CC1 introduction enhanced neurite growth, RNAi-mediated knockdown of RB1CC1 or rapamycin treatment caused neurite atrophy and apoptosis due to mTOR signaling reduction in the differentiated Neuro-2a cells. Both TSC1 and RB1CC1 were equally functional and maintained mTOR signaling, indicated by phospho-S6 (Ser240/244) expression in 69% of Alzheimer's (9/13 cases) and 100% of normal brains (6/6 cases). However, scanty RB1CC1 expression, less than TSC1, caused phospho-S6 disappearance in 31% of Alzheimer's tissues (4/13 cases). These findings suggest that RB1CC1 insufficiency may result in mTOR signaling repression through unbalanced TSC1 abundance and may induce neuronal atrophy. These observations may have implications for the pathogenesis of Alzheimer's disease.
MeSH term(s)	Alzheimer Disease/pathology ; Animals ; Atrophy/etiology ; Brain/pathology ; Cell Cycle/drug effects ; Cell Death/drug effects ; Cell Line, Tumor ; Embryo, Mammalian ; Humans ; Immunosuppressive Agents/pharmacology ; Intracellular Signaling Peptides and Proteins/deficiency ; Mice ; Neuroblastoma ; Neurons/drug effects ; Neurons/pathology ; Protein Kinases/metabolism ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Sirolimus/pharmacology ; TOR Serine-Threonine Kinases ; Transfection/methods ; Tumor Suppressor Proteins/metabolism
Chemical Substances	Immunosuppressive Agents ; Intracellular Signaling Peptides and Proteins ; Rb1cc1 protein, mouse ; Tumor Suppressor Proteins ; tuberous sclerosis complex 1 protein ; Protein Kinases (EC 2.7.-) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; mTOR protein, mouse (EC 2.7.1.1) ; Sirolimus (W36ZG6FT64)
Language	English
Publishing date	2007-09-07
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2007.06.075
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Article ; Online: Somatic uniparental disomy of Chromosome 16p in hemimegalencephaly.

Griffin, Nicole G / Cronin, Kenneth D / Walley, Nicole M / Hulette, Christine M / Grant, Gerald A / Mikati, Mohamad A / LaBreche, Heather G / Rehder, Catherine W / Allen, Andrew S / Crino, Peter B / Heinzen, Erin L

Cold Spring Harbor molecular case studies

2017 Volume 3, Issue 5

Abstract: Hemimegalencephaly (HME) is a heterogeneous cortical malformation characterized by enlargement of one cerebral hemisphere. Somatic variants in mammalian target of rapamycin (mTOR) regulatory genes have been implicated in some HME cases; however, ∼70% ... ...

Abstract	Hemimegalencephaly (HME) is a heterogeneous cortical malformation characterized by enlargement of one cerebral hemisphere. Somatic variants in mammalian target of rapamycin (mTOR) regulatory genes have been implicated in some HME cases; however, ∼70% have no identified genetic etiology. Here, we screened two HME patients to identify disease-causing somatic variants. DNA from leukocytes, buccal swabs, and surgically resected brain tissue from two HME patients were screened for somatic variants using genome-wide genotyping arrays or sequencing of the protein-coding regions of the genome. Functional studies were performed to evaluate the molecular consequences of candidate disease-causing variants. Both HME patients evaluated were found to have likely disease-causing variants in DNA extracted from brain tissue but not in buccal swab or leukocyte DNA, consistent with a somatic mutational mechanism. In the first case, a previously identified disease-causing somatic single nucleotide in
MeSH term(s)	Alleles ; Brain/cytology ; Child, Preschool ; Chromosomes/genetics ; Chromosomes, Human, Pair 16/genetics ; DNA/genetics ; DNA Methylation/genetics ; Female ; Genomic Imprinting ; Genotype ; Hemimegalencephaly/genetics ; Humans ; Infant ; Uniparental Disomy/genetics
Chemical Substances	DNA (9007-49-2)
Language	English
Publishing date	2017-09-01
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2835759-0
ISSN	2373-2873 ; 2373-2873
ISSN (online)	2373-2873
ISSN	2373-2873
DOI	10.1101/mcs.a001735
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Article ; Online: Sudden death from diffuse leptomeningeal oligodendrogliomatosis.

Reynolds, Renee M / Boswell, Elizabeth / Hulette, Christine M / Cummings, Thomas J / Haglund, Michael M / Hulette, Christine M / Cumm Ings, Thomas J

Journal of neurosurgery. Spine

2011 Volume 15, Issue 6, Page(s) 625–629

Abstract: In this paper the authors describe the rare disorder of diffuse leptomeningeal oligodendrogliomatosis in a patient with an oligodendroglioma of the cauda equina who died suddenly. Reviewing this uncommon pathological entity is important so that it can be ...

Abstract	In this paper the authors describe the rare disorder of diffuse leptomeningeal oligodendrogliomatosis in a patient with an oligodendroglioma of the cauda equina who died suddenly. Reviewing this uncommon pathological entity is important so that it can be recognized and treated appropriately. This young, otherwise healthy woman with initial symptoms of low-back pain had a mass lesion of the cauda equina. During a workup, profound refractory intracranial hypertension suddenly developed despite aggressive surgical and medical intervention. Autopsy revealed a spinal cord oligodendroglioma with diffuse leptomeningeal oligodendrogliomatosis of the brain and spinal cord. Given the unforeseen outcome in this patient, this entity, although rare, should be considered in patients with similar presentations and addressed early to prevent similar outcomes. A review of the details of this case as well as the literature is presented below.
MeSH term(s)	Adult ; Death, Sudden/pathology ; Fatal Outcome ; Female ; Humans ; Magnetic Resonance Imaging ; Meningeal Neoplasms/pathology ; Meningeal Neoplasms/surgery ; Neoplasm Invasiveness/pathology ; Oligodendroglioma/pathology ; Oligodendroglioma/surgery ; Severity of Illness Index ; Spinal Cord Neoplasms/pathology ; Spinal Cord Neoplasms/surgery ; Tomography, X-Ray Computed
Language	English
Publishing date	2011-12
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	2158643-3
ISSN	1547-5646 ; 1547-5654
ISSN (online)	1547-5646
ISSN	1547-5654
DOI	10.3171/2011.7.SPINE10728
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Article ; Online: Differential gene expression in dentate granule cells in mesial temporal lobe epilepsy with and without hippocampal sclerosis.

Griffin, Nicole G / Wang, Yu / Hulette, Christine M / Halvorsen, Matt / Cronin, Kenneth D / Walley, Nicole M / Haglund, Michael M / Radtke, Rodney A / Skene, J H Pate / Sinha, Saurabh R / Heinzen, Erin L

Epilepsia

2016 Volume 57, Issue 3, Page(s) 376–385

Abstract: Objective: Hippocampal sclerosis is the most common neuropathologic finding in cases of medically intractable mesial temporal lobe epilepsy. In this study, we analyzed the gene expression profiles of dentate granule cells of patients with mesial ... ...

Abstract	Objective: Hippocampal sclerosis is the most common neuropathologic finding in cases of medically intractable mesial temporal lobe epilepsy. In this study, we analyzed the gene expression profiles of dentate granule cells of patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis to show that next-generation sequencing methods can produce interpretable genomic data from RNA collected from small homogenous cell populations, and to shed light on the transcriptional changes associated with hippocampal sclerosis. Methods: RNA was extracted, and complementary DNA (cDNA) was prepared and amplified from dentate granule cells that had been harvested by laser capture microdissection from surgically resected hippocampi from patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis. Sequencing libraries were sequenced, and the resulting sequencing reads were aligned to the reference genome. Differential expression analysis was used to ascertain expression differences between patients with and without hippocampal sclerosis. Results: Greater than 90% of the RNA-Seq reads aligned to the reference. There was high concordance between transcriptional profiles obtained for duplicate samples. Principal component analysis revealed that the presence or absence of hippocampal sclerosis was the main determinant of the variance within the data. Among the genes up-regulated in the hippocampal sclerosis samples, there was significant enrichment for genes involved in oxidative phosphorylation. Significance: By analyzing the gene expression profiles of dentate granule cells from surgically resected hippocampal specimens from patients with mesial temporal lobe epilepsy with and without hippocampal sclerosis, we have demonstrated the utility of next-generation sequencing methods for producing biologically relevant results from small populations of homogeneous cells, and have provided insight on the transcriptional changes associated with this pathology.
MeSH term(s)	Adult ; Dentate Gyrus/metabolism ; Dentate Gyrus/pathology ; Dentate Gyrus/surgery ; Electroencephalography/methods ; Epilepsy, Temporal Lobe/diagnosis ; Epilepsy, Temporal Lobe/metabolism ; Epilepsy, Temporal Lobe/surgery ; Female ; Gene Expression Regulation ; Hippocampus/metabolism ; Hippocampus/pathology ; Hippocampus/surgery ; Humans ; Male ; Middle Aged ; Principal Component Analysis/methods ; Sclerosis ; Young Adult
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	216382-2
ISSN	1528-1167 ; 0013-9580
ISSN (online)	1528-1167
ISSN	0013-9580
DOI	10.1111/epi.13305
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Article: Adult cases of leukoencephalopathy, cerebral calcifications, and cysts: expanding the spectrum of the disorder.

Kleinschmidt-Demasters, Bette Kay / Cummings, Thomas J / Hulette, Christine M / Morgenlander, Joel C / Corboy, John R

Journal of neuropathology and experimental neurology

2009 Volume 68, Issue 4, Page(s) 432–439

Abstract: Leukoencephalopathy with cerebral calcifications and cysts (LCC) was first reported in children who developed cognitive decline and variable extrapyramidal, cerebellar, and pyramidal signs, with or without seizures. Leukoencephalopathy with cerebral ... ...

Abstract	Leukoencephalopathy with cerebral calcifications and cysts (LCC) was first reported in children who developed cognitive decline and variable extrapyramidal, cerebellar, and pyramidal signs, with or without seizures. Leukoencephalopathy with cerebral calcifications and cysts is characterized by progressive formation of brain cysts that can generate a mass effect simulating a neoplasm. Retinal changes that overlap with Coats disease, a microangiopathy with retinal telangiectasias and exudates, may also occur. We and others have reported LCC cases in adults. Neuroimaging shows diffuse leukoencephalopathy, multifocal calcifications especially of deep gray and white matter, multifocal enhancement, and variably sized cysts that may require surgical decompression. Biopsies adjacent to cysts have shown angiomatous and/or severely hyalinized blood vessels surrounded by myelin loss and gliosis, calcifications, and Rosenthal fibers. We report 2 additional adult-onset cases of LCC. Case 1 is a 40-year-old man who developed neurological symptoms and cirrhosis and died of acute gastrointestinal bleeding; he had numerous retinal microinfarcts at autopsy. Case 2 is a 55-year-old woman who was found by chance to have LCC; one and a half years later, her course remains benign. These cases expand the spectrum of adult-onset LCC, the etiology of which is unknown.
MeSH term(s)	Adult ; Brain/pathology ; Brain/physiopathology ; Calcinosis/complications ; Calcinosis/pathology ; Cysts/complications ; Cysts/pathology ; Dementia, Vascular/complications ; Dementia, Vascular/pathology ; Female ; Humans ; Magnetic Resonance Imaging ; Male ; Middle Aged
Language	English
Publishing date	2009-04
Publishing country	England
Document type	Case Reports ; Journal Article
ZDB-ID	3088-0
ISSN	1554-6578 ; 0022-3069
ISSN (online)	1554-6578
ISSN	0022-3069
DOI	10.1097/NEN.0b013e31819fd897
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