0000000000088303

AUTHOR

Heiko Braak

showing 15 related works from this author

Silver Impregnation of Alzheimer's Neurofibrillary Changes Counterstained for Basophilic Material and Lipofuscin Pigment

1988

A method is described in which selective silver staining of Alzheimer's neurofibrillary changes is combined with staining of cell nuclei, Nissl material, and lipofuscin granules. Formalin fixed, paraffin embedded sections of human autopsy tissue are silver stained according to a method proposed by Gallyas. Lipofuscin is stained by crotonaldehyde fuchsin following performic acid oxidation. Nissl substance is visualized by either Darrow red or gallocyanin-chrome alum staining. Architectonic units showing the specific pathology and the neuronal types prone to develop the neurofibrillary changes can be recognized using this technique.

Pathologymedicine.medical_specialtySilverALIZARIN REDLipofuscinLipofuscinSilver stainPigmentsymbols.namesakechemistry.chemical_compoundAlzheimer DiseasemedicineHumansPerformic acidStaining and LabelingChemistryMiddle AgedStainingBasophilicnervous systemNissl Bodiesvisual_artNeurofibrilsvisual_art.visual_art_mediumNissl bodysymbolsFemalesense organsAnatomyStain Technology
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Klinische Aspekte der "argyrophilic grain disease"

2000

Argyrophilic grain disease (AGD) is a frequently occurring degenerative illness of the aging human brain. It is accompanied by progressive pathological alterations of the cytsokeleton which are traceable to an abnormal phosphorylation of the microtubule associated tau protein. Histologically, it is possible with the help of suitable staining techniques to identify pathognomonic spindle-shaped cellular inclusions (argyrophilic grains). These cellular inclusions display a typical cortical as well as subcortical distribution pattern. The goal of the present study is the retrospective evaluation of the clinical findings from 53 individuals with neuropathologically demonstrable AGD-related chang…

Pathologymedicine.medical_specialtyNeurologybiologybusiness.industryTau proteinNeurodegenerationGeneral MedicineDiseaseHuman brainmedicine.diseasePsychiatry and Mental healthmedicine.anatomical_structureNeurologyPathognomonicbiology.proteinMedicineDementiaNeurology (clinical)businessPathologicalDer Nervenarzt
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Neurofibrillary tangles and neuropil threads as a cause of dementia in Parkinson’s disease

1997

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most common age-related degenerative disorders of the human brain. Both diseases involve multiple neuronal systems and are the consequences of cytoskeletal abnormalities. In AD susceptible neurons produce neurofibrillary changes, while in Parkinson’s disease, they develop Lewy bodies. In AD six developmental stages can be distinguished on account of the predictable manner in which the neurofibrillary changes spread across the cerebral cortex. During the course of PD numerous limbic determined parts of the brain undergo specific lesions regulating endocrine and autonomic functions. In general, the extranigral destructions are in t…

Parkinson's diseaseDegenerative Disorderbusiness.industryDiseaseHuman brainEntorhinal cortexmedicine.diseaseNeuropil threadmedicine.anatomical_structureCerebral cortexmedicineDementiabusinessNeuroscience
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Amygdala pathology in Parkinson's disease.

1994

The amygdala undergoes severe pathological changes during the course of Parkinson's disease (PD). Lewy bodies and Lewy neurites are distributed in a specific manner throughout the nuclear complex. The lesional pattern displays only minor interindividual variation. The most prominent changes occur in the accessory cortical and central nuclei. The cortical, accessory basal and granular nuclei show less severe alterations, while the basal and lateral nuclei, as well as the intercalated cell masses, generally remain uninvolved. The amygdala receives a broad range of afferents, allowing integration of exteroceptive information with interoceptive data. It generates major projections to the isocor…

MalePathologymedicine.medical_specialtyParkinson's diseaseLewy bodyHippocampusParkinson DiseaseBiologyMiddle Agedmedicine.diseaseAmygdalaAmygdalaPathology and Forensic MedicineCellular and Molecular NeuroscienceBasal (phylogenetics)Limbic systemmedicine.anatomical_structureDegenerative diseasemedicineHumansFemaleNeurology (clinical)Prefrontal cortexAgedActa neuropathologica
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Pigment variant of neuronal ceroid-lipofuscinosis

1995

A 6-year-old girl had progressive ataxia, and visual disturbances resulting in blindness. She died in her sleep at age 22 years. She shared with her sister and paternal relatives bilateral pes cavus deformities and impaired deep-tendon reflexes which suggested Charcot-Marie-Tooth disease. Her sister, who also had both polyneuropathy and a progressive central nervous system (CNS) disease, did not have pigmentary retinopathy. At autopsy, the patient was found to have neuronal ceroid-lipofuscinosis (NCL) marked by intraneuronal accumulation of autofluorescent granular lipopigments in ballooned perikarya and conspicuous extraneuronal pigmentation of subcortical grey matter, but without axonal s…

Malemedicine.medical_specialtyPathologyPostmortem studiesNeurologyCentral nervous systemAutopsyBiologyGrey matterEpitheliumNuclear FamilyDiagnosis DifferentialCharcot-Marie-Tooth DiseaseNeuronal Ceroid-LipofuscinosesmedicineNeuropilHumansChildGenetics (clinical)Cerebral CortexNeuronsPigmentationPigments BiologicalAnatomymedicine.diseaseMicroscopy ElectronKidney Tubulesmedicine.anatomical_structureSpinal CordFemaleNeuronal ceroid lipofuscinosisPolyneuropathyAmerican Journal of Medical Genetics
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Pattern of brain destruction in Parkinson's and Alzheimer's diseases

1996

Alzheimer's disease (AD) and Parkinson's disease (PD) are the most common age-related degenerative disorders of the human brain. Both diseases involve multiple neuronal systems and are the consequences of cytoskeletal abnormalities which gradually develop in only a small number of neuronal types. In AD, susceptible neurons produce neurofibrillary tangles (NFTs) and neuropil threads (NTs), while in PD, they develop Lewy bodies (LBs) and Lewy neurites (LNs). The specific lesional pattern of both illnesses accrues slowly over time and remains remarkably consistent across cases. In AD, six developmental stages can be distinguished on account of the predictable manner in which the neurofibrillar…

AgingPathologymedicine.medical_specialtyParkinson's diseaseModels NeurologicalLimbic systemAlzheimer DiseaseLimbic SystemmedicineHumansBiological PsychiatryNeocortexLewy bodyBrainParkinson DiseaseNeurofibrillary tangleHuman brainmedicine.diseasePsychiatry and Mental healthmedicine.anatomical_structurenervous systemNeurologyCerebral cortexLewy neuriteNeurology (clinical)PsychologyNeuroscienceJournal of Neural Transmission
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Topical Review: Functional Anatomy of Human Hippocampal Formation and Related Structures

1996

Data on the internal organization, and neuronal connections of the human hippocampal formation and related structures of the limbic system are briefly reviewed. In the healthy brain, somatosensory, visual, and auditory input proceeds through neocortical core and belt fields to a variety of association areas, and from here the data is transported via long cortico-cortical pathways to the extended prefrontal association cortex. Tracts generated from this highest organizational level of the brain guide the data via the frontal belt (premotor cortex) to the frontal core (primary motor area). The striatal and cerebellar loops provide the major routes for this data transfer. The main components o…

Working memory05 social sciencesSensory systemHippocampal formationSomatosensory system050105 experimental psychologyPremotor cortex03 medical and health sciences0302 clinical medicineLimbic systemmedicine.anatomical_structurenervous systemPediatrics Perinatology and Child Healthmedicine0501 psychology and cognitive sciencesNeurology (clinical)Prefrontal cortexPsychologyConsumer neuroscienceNeurosciencepsychological phenomena and processes030217 neurology & neurosurgeryJournal of Child Neurology
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Gastric α-synuclein immunoreactive inclusions in Meissner's and Auerbach's plexuses in cases staged for Parkinson's disease-related brain pathology

2005

The progressive degenerative process associated with sporadic Parkinson's disease (sPD) is characterized by formation of alpha-synuclein-containing inclusion bodies in a few types of projection neurons in both the enteric and central nervous systems (ENS and CNS). In the brain, the process apparently begins in the brainstem (dorsal motor nucleus of the vagal nerve) and advances through susceptible regions of the basal mid-and forebrain until it reaches the cerebral cortex. Anatomically, all of the vulnerable brain regions are closely interconnected. Whether the pathological process begins in the brain or elsewhere in the nervous system, however, is still unknown. We therefore used immunocyt…

MaleNervous systemProtein FoldingPathologymedicine.medical_specialtyPrionsModels NeurologicalCentral nervous systemMyenteric PlexusBiologyAxonal TransportCentral nervous system diseaseNeural PathwaysDisease Transmission InfectiousmedicineHumansAgedAged 80 and overInclusion BodiesNeuronsGeneral NeuroscienceBrainParkinson DiseaseVagus NerveSubmucous PlexusMiddle Agedmedicine.diseasemedicine.anatomical_structureDorsal motor nucleusGastric MucosaCerebral cortexForebrainalpha-SynucleinFemaleEnteric nervous systemBrainstemNerve NetNeuroscienceNeuroscience Letters
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Fabry Disease With Concomitant Lewy Body Disease

2019

AbstractAlthough Gaucher disease can be accompanied by Lewy pathology (LP) and extrapyramidal symptoms, it is unknown if LP exists in Fabry disease (FD), another progressive multisystem lysosomal storage disorder. We aimed to elucidate the distribution patterns of FD-related inclusions and LP in the brain of a 58-year-old cognitively unimpaired male FD patient suffering from predominant hypokinesia. Immunohistochemistry (CD77, α-synuclein, collagen IV) and neuropathological staging were performed on 100-µm sections. Tissue from the enteric or peripheral nervous system was unavailable. As controls, a second cognitively unimpaired 50-year-old male FD patient without LP or motor symptoms and 3…

complications [Lewy Body Disease]MalePathologyAutopsyDisease0302 clinical medicineHypokinesiapathology [Brain]Lysosomal storage diseasespathology [Neurons]metabolism [alpha-Synuclein]metabolism [Fabry Disease]pathology [Astrocytes]Neuronsα-Synuclein0303 health sciencesParkinsonismTrihexosylceramidesBrainGeneral MedicineMiddle AgedParkinson diseasecomplications [Fabry Disease]Neurologymetabolism [Neurons]alpha-Synucleinmedicine.symptomLewy Body Diseasemedicine.medical_specialtymetabolism [Lewy Body Disease]Context (language use)Substantia nigrametabolism [Trihexosylceramides]Pathology and Forensic Medicineblood supply [Brain]03 medical and health sciencesCellular and Molecular Neuroscienceα-Galactosidase AmedicineHumansddc:610030304 developmental biologypathology [Lewy Bodies]Fabry diseasebusiness.industryPars compactapathology [Lewy Body Disease]Lewy bodies/neuritesOriginal Articlesmetabolism [Lewy Bodies]medicine.diseaseFabry diseasemetabolism [Brain]AstrocytesLewy BodiesNeurology (clinical)CD77pathology [Fabry Disease]business030217 neurology & neurosurgeryJournal of Neuropathology and Experimental Neurology
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Allocortical neurofibrillary changes in progressive supranuclear palsy.

1992

Silver techniques for intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) and extracellular A4-amyloid deposits were used to examine lesions of the cerebral cortex in six cases of progressive supranuclear palsy (three were mentally unimpaired and three showed moderate degrees of dementia). Deposits of A4-amyloid protein occurred in small numbers or were absent. Neurofibrillary tangles and neuropil threads were present in all cases and were largely confined to the allocortex. A characteristic pattern of changes was found in the entorhinal cortex. The three mentally unimpaired individuals had mild cortical changes virtually confined to the transentorhinal r…

MalePathologymedicine.medical_specialtyAmyloidSilver StainingHippocampusBiologyHippocampal formationHippocampusPathology and Forensic MedicineProgressive supranuclear palsyCellular and Molecular NeuroscienceAlzheimer DiseasemedicineHumansAgedCerebral CortexAllocortexBrainNeurofibrillary tangleNeurofibrillary TanglesMiddle AgedPerforant pathmedicine.diseaseEntorhinal cortexmedicine.anatomical_structureCerebral cortexFemaleNeurology (clinical)Supranuclear Palsy ProgressiveActa neuropathologica
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Stanley Fahn Lecture 2005: The staging procedure for the inclusion body pathology associated with sporadic Parkinson's disease reconsidered.

2006

The synucleinopathy known as sporadic Parkinson's disease (PD) is a multisystem disorder that severely damages predisposed nerve cell types in circumscribed regions of the human nervous system. A recent staging procedure for the inclusion body pathology associated with PD proposes that, in the brain, the pathological process (formation of proteinaceous intraneuronal Lewy bodies and Lewy neurites) begins at two sites and continues in a topographically predictable sequence in six stages, during which components of the olfactory, autonomic, limbic, and somatomotor systems become progressively involved. In stages 1 to 2, the Lewy body pathology is confined to the medulla oblongata/pontine tegme…

Inclusion BodiesPathologymedicine.medical_specialtyParkinson's diseaseLewy bodyAnatomical pathologySubstantia nigraParkinson Diseasemedicine.diseaseCentral nervous system diseaseDegenerative diseasenervous systemNeurologyForebrainmedicineTegmentumDisease ProgressionAnimalsHumansNeurology (clinical)PsychologyNeuroscienceMovement disorders : official journal of the Movement Disorder Society
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Isocortical Pathology in Type C Niemann-Pick Disease

1983

A case of Niemann-Pick disease was examined with Golgi preparations and a transparent Golgi impregnation counterstained for intraneuronal pigment deposits. There was a specific type of storage of unmetabolized substrate restricted to certain nerve cell types. The most conspicuous changes in the isocortex were: 1) dilated axonal segments in layer IIIab pyramidal cells filled with storage material; the volume of these axonal expansions often exceeded that of the soma; 2) distension of layer IIIc, layer V, and layer VIa pyramidal cell perikarya with storage material; 3) new formation, elongation, and vertical orientation of basal dendrites in layer V pyramidal cells; 4) well-preserved pyramida…

AdultCell typePathologymedicine.medical_specialtyBiologyDistensionPathology and Forensic MedicineLipofuscinCellular and Molecular Neurosciencesymbols.namesakemedicineHumansCerebral CortexNiemann-Pick DiseasesStaining and LabelingDendritesGeneral MedicineGolgi apparatusmedicine.diseaseAxonsmedicine.anatomical_structureNeurologyHepatic stellate cellsymbolsFemaleNeurology (clinical)Pyramidal cellNiemann–Pick diseaseLayer (electronics)Journal of Neuropathology and Experimental Neurology
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Alzheimer's disease: Amyloid deposits in the cerebellar cortex

1989

Pathologymedicine.medical_specialtyNeurologyAmyloidbusiness.industryGeneral NeuroscienceDiseasePsychiatry and Mental healthNeurologyCerebellar cortexmedicineNeurology (clinical)Senile plaquesbusinessBiological PsychiatryJournal of Neural Transmission - Parkinson's Disease and Dementia Section
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Alzheimer-related changes in the presubicular region

1989

Psychiatry and Mental healthmedicine.medical_specialtyNeurologyNeurologybusiness.industryGeneral NeurosciencemedicineNeurology (clinical)businessNeuroscienceBiological PsychiatryJournal of Neural Transmission - Parkinson's Disease and Dementia Section
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Alzheimer's disease: amyloid plaques in the cerebellum

1989

Two specific silver-staining methods demonstrating either extracellular amyloid and/or precursors of amyloid or intraneuronal neurofibrillary changes were used to examine cerebellar pathology in cases of presenile and senile dementia of the Alzheimer type, cases of Down's syndrome, and non-demented controls. The sensitivity of the techniques permitted visualization of large numbers of amyloid deposits in the cerebellar cortex of demented individuals. Similarly large numbers of amyloid deposits were not found in the cerebella of non-demented individuals. Neurofibrillary changes were absent. The majority of amyloid plaques occurred in the molecular layer. Quite a number of these displayed lar…

AdultMaleCerebellumPathologymedicine.medical_specialtyAdolescentAmyloidGranular layerBiologyWhite matterAlzheimer DiseaseCerebellar DiseasesCerebellummental disordersmedicineHumansSenile plaquesAgedAged 80 and overInclusion BodiesAmyloidosisAmyloidosisMiddle Agedmedicine.diseasemedicine.anatomical_structureNeurologyCerebellar cortexFemaleNeurology (clinical)Down SyndromeAlzheimer's diseaseNeuroscienceJournal of the Neurological Sciences
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