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Biomedical subjects

E Braak

Publications and source records attributed to E Braak.

At least 73 records · Page 4Linked to original sources
PubMed1993

Parvalbumin-immunoreactive structures of the adult human entorhinal and transentorhinal region.

Parvalbumin-immunoreactive structures in the entorhinal and transentorhinal region of the adult human brain were studied using the avidin-biotin-peroxidase technique. Parvalbumin-immunoreactive neurons and fibers (axons) were present in all layers (layer nomenclature according to Rose, 1927). The density of fibers was high in the islands of the superficial cell layer pre-alpha and in layer pre-beta and still heavier in pre-gamma. In the subjacent lamina dissecans it diminished abruptly and remained low in all layers of the internal principal stratum (layers pri-alpha, -beta, -gamma). This low density of fibers facilitated recognition of axon cartridges in layers pri-alpha and pri-gamma. Axon cartridges were also present within layers pre-beta and pre-gamma but were obscured by the dense fiber network there. Parvalbumin immunoreactivity was observed in the nerve cell soma and throughout the dendritic tree allowing the distinction of numerous nerve cell types. All parvalbumin-immunoreactive neurons belonged to the class of nonpyramidal neurons. Their lipofuscin pigment patterns differed distinctly from that of the pyramidal and modified pyramidal neurons. Based on their location, soma size, and dendritic arborization, they were grouped as large, medium-sized, and small neurons either of the multipolar or bipolar (vertical or horizontal) type. One type could be identified as an axo-axonic neuron, more specifically as a chandelier neuron generating axon cartridges. The dense fiber net within layer pre-gamma suggested the existence of another neuronal type, probably a neuron with an extended axonal ramification. The identified neurons were compared to neuronal types described in the literature from Golgi studies.

Adult↗
PubMed1993

Staging of Alzheimer-related cortical destruction.

The gradual intraneuronal accumulation of an insoluble fibrous material which partly consists of abnormally phosphorylated tau protein (neurofibrillary change) represents an important neuropathological hallmark of Alzheimer's disease. Neurofibrillary tangles and neuropil threads formed from this material develop in only a few types of cortical pyramidal cells. The first changes are seen in the entorhinal cortex. The destructive process then spreads into the hippocampal formation and eventually encroaches upon the isocortex. This sequence of events permits the distinction of six stages with a progressive increase in the severity of cortical destruction. The entorhinal region serves as an important interface between the isocortex and hippocampus. This interface function is markedly impaired due to the early deterioration of the entorhinal cortex. Severe entorhinal involvement is considered to represent the morphological counterpart of clinically incipient Alzheimer's disease. Similar changes are found in mentally impaired individuals suffering from Parkinson's disease or progressive supranuclear palsy.

Aged↗
PubMed1992

Allocortical neurofibrillary changes in progressive supranuclear palsy.

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 region while all of the demented patients showed severe destruction of the superficial cellular layer in both the transentorhinal and entorhinal region. This pattern of allocortical destruction closely resembles that seen in clinically incipient Alzheimer's disease or in mentally impaired cases of Parkinson's disease. The entorhinal region receives dense input from isocortical association areas and projects via the perforant path to the hippocampal formation. The cells of origin of major portions of the perforant path are located within the superficial entorhinal cellular layer. Destruction of this layer partially or totally disconnects the hippocampus from the isocortex. The specific pattern of entorhinal destruction is considered to contribute to cognitive impairment and personality changes, frequently seen in patients with progressive supranuclear palsy.

Aged↗
PubMed1992

The human entorhinal cortex: normal morphology and lamina-specific pathology in various diseases.

The entorhinal territory consists of the entorhinal and transentorhinal regions spreading over the ambient gyrus and anterior portions of the parahippocampal gyrus. The transentorhinal region mediates between the adjoining temporal isocortex laterally and the entorhinal region medially. The entorhinal cortex consists of a molecular layer, followed by an external principal stratum, a cell-sparse lamina dissecans, an internal principal stratum and--within the underlying white matter--a profound cellular layer. The principal strata can each be divided into three layers Pre alpha, beta, gamma, and Pri alpha, beta, gamma. Data obtained from experimental investigations in monkeys reveal that the entorhinal territory serves as a relay station for information from both isocortical association areas and centers of the limbic system. After processing within the entorhinal cortex, this information is transferred to the hippocampal formation via the perforant path. Pathological changes within the entorhinal territory impair this continuous data transfer and contribute to a decline of cognitive functions. Entorhinal involvement associated with impaired cognitive functions is described in cases of Alzheimer's disease, Parkinson's disease, progressive supranuclear palsy, dementia with argyrophilic grains and Huntington's disease.

Central Nervous System Diseases↗
PubMed1992

Anatomy of the human hypothalamus (chiasmatic and tuberal region).

The hypothalamus sensu stricto consists of the chiasmatic, the tuberal and the mamillary region. The present study is confined to the poorly myelinated chiasmatic and tuberal region. Both regions harbor many nuclear grays with relatively clear-cut boundaries embedded in an ill-defined nerve cell assembly referred to as the hypothalamic gray. Prominent components of the chiasmatic region are the magnocellular neurosecretory complex (supraoptic nucleus, paraventricular nucleus, accessory neurosecretory nucleus), the sexually dimorphic intermediate nucleus, the suprachiasmatic and retrochiasmatic nuclei. The dominating structure of the tuberal region is the complex of the ventromedial, posteromedial and dorsomedial nuclei supplemented by the periventricular and infundibular nuclei. Lateral portions of the tuber cinereum harbor the lateral tuberal nucleus and the tuberomamillary nucleus. The lateral tuberal nucleus exhibits pronounced cell loss in Huntington's chorea and is also severely involved in cases of dementia with argyrophilic grains. The large nerve cells of the tuberomamillary nucleus show particularly severe affection in both Alzheimer's (intraneuronal neurofibrillary changes) and Parkinson's disease (Lewy bodies).

Female↗
PubMed1992

Allocortical involvement in Huntington's disease.

Seven brains of individuals who had suffered from Huntington's disease and seven control brains were examined. Preparations stained for Nissl material and lipofuscin pigment revealed a characteristic layer-specific loss of nerve cells in two allocortical areas, the entorhinal region and the subiculum. The most severe changes occurred in the entorhinal layer Pri-gamma while layer Pre-alpha, layer Pre-gamma and the subiculum showed less severe alterations.

Cell Survival↗
PubMed1991

Glutamic acid decarboxylase (GAD)-immunoreactive structures in the adult human lateral geniculate nucleus.

The distribution of glutamic acid decarboxylase (GAD)-like immunoreactivity in the lateral geniculate nucleus (LGN) of the human adult was studied in vibratome sections (50-60 microns thick) using the avidinbiotin-peroxidase method. The tissue was obtained at autopsy from five individuals without any known neurological disorders. Only few GAD-immunoreactive neurons were present in the layers of the LGN, even less in the interlaminar zones. The numerical density of GAD-immunoreactive neurons and puncta (probably synaptic boutons and or cross sectioned cell processes) in the magnocellular layers was larger than in the parvocellular layers. Furthermore, no striking differences between the individual parvocellular layers were noted. The immunoreactive somata were polygonal or triangular, occasionally pear-shaped, and ranged in size from 15 to 25 microns. They gave off two to four short, thick, straight primary dendrites. A preferred orientation of dendrites was not recognized. After bleaching the chromogen 4-chloro-1-naphthol and staining for lipofuscin pigment granules and basophilic material, 254 unequivocally relocated GAD-immunoreactive nerve cells could be classified as belonging to the lipofuscin pigment granules-containing class of interneurons.

Adult↗
PubMed1991

Parvalbumin-immunoreactive structures in the hippocampus of the human adult.

Parvalbumin-immunoreactive structures in the fascia dentata and Ammon's horn of the adult human brain were studied using the avidin-biotin-peroxidase technique. Thin fibres (probably axons) were found to form dense networks throughout the cellular layers. Parvalbumin immunoreactivity is observed in even distal portions of nerve cell processes. The excellent quality of the immunoreaction renders the distinction of a large number of possible neuronal types. All parvalbumin-immunoreactive neurons belong to the class of non-granule cells in the fascia dentata and non-pyramidal neurons in Ammon's horn. The fascia dentata harbours four types of neurons in the molecular layer, one type within the granule cell layer and four types in the plexiform layer. The frequently described basket cells are contained in the group of immunoreactive non-granule cells in the plexiform layer. In field CA4 two neuronal types can be distinguished. Field CA3 reveals a slender cell type in the stratum radiatum, three types in the pyramidal cell layer and three types in the stratum oriens. In field CA2 three neuronal types can be differentiated in the stratum pyramidale. The extended field CA1 is endowed with two types of nerve cells within the stratum moleculare, two types in the stratum radiatum, five neuronal types in the stratum pyramidale, and one spindle-shaped type in the stratum oriens. The morphological features of parvalbumin-immunoreactive neuronal types in the adult human brain are compared with those found in Golgi-studies of mostly young animals or in labelling experiments. This study serves as a basis for further analyzes involving specific diseases such as Alzheimer's disease or epilepsy, where it needs to be clarified to which extent certain neuronal types are afflicted.

Adult↗
PubMed1991

Alzheimer's disease affects limbic nuclei of the thalamus.

Sensitive silver techniques for amyloid and neurofibrillary changes were applied to examine the pathological changes revealed by limbic nuclei of the thalamus in Alzheimer's disease. Large numbers of extracellular amyloid deposits occurred in almost all thalamic nuclei. The antero-ventral nucleus harbored numerous large globular patches, other areas contained more densely packed and smaller deposits, while narrow zones of gray matter subjacent to the ependymal lining of the third ventricle remained virtually devoid of amyloid. Intraneuronal neurofibrillary changes were encountered in the form of distended argyrophilic processes covering the medial convexity of the antero-ventral nucleus. Similar structures, although in considerably lesser density, occurred in the laterally adjoining reticular nucleus. The anterior nuclear complex, the latero-dorsal nucleus, portions of the intralaminar complex, the paraventricular and reuniens nucleus contained numerous neurofibrillary tangles and neuropil threads. The antero-dorsal nucleus showed the most severe involvement. At first glance, the thalamus appeared to be only mildly affected by Alzheimer's disease. Closer inspection revealed that severe changes were confined to only a few limbic nuclei. These changes were virtually identical in amount, type and location in all cases of severe Alzheimer's disease studied. It is assumed that these changes considerably hamper the transport of information through limbic circuits.

Aged↗
PubMed1991

Neuropathological stageing of Alzheimer-related changes.

Eighty-three brains obtained at autopsy from nondemented and demented individuals were examined for extracellular amyloid deposits and intraneuronal neurofibrillary changes. The distribution pattern and packing density of amyloid deposits turned out to be of limited significance for differentiation of neuropathological stages. Neurofibrillary changes occurred in the form of neuritic plaques, neurofibrillary tangles and neuropil threads. The distribution of neuritic plaques varied widely not only within architectonic units but also from one individual to another. Neurofibrillary tangles and neuropil threads, in contrast, exhibited a characteristic distribution pattern permitting the differentiation of six stages. The first two stages were characterized by an either mild or severe alteration of the transentorhinal layer Pre-alpha (transentorhinal stages I-II). The two forms of limbic stages (stages III-IV) were marked by a conspicuous affection of layer Pre-alpha in both transentorhinal region and proper entorhinal cortex. In addition, there was mild involvement of the first Ammon's horn sector. The hallmark of the two isocortical stages (stages V-VI) was the destruction of virtually all isocortical association areas. The investigation showed that recognition of the six stages required qualitative evaluation of only a few key preparations.

Aged↗
PubMed1991

Calbindin-D-28k-like immunoreactive structures in the olfactory bulb and anterior olfactory nucleus of the human adult: distribution and cell typology--partial complementarity with parvalbumin.

Calbindin-D-28k and parvalbumin are calcium-binding proteins. The laminar distribution and morphological features of calbindin-D-28k-like immunoreactive structures were studied in 60-microns-thick sections of the human olfactory bulb. Except for the olfactory nerve layer, immunoreactive neurons were present in all layers of the olfactory bulb. They reached highest densities in the external plexiform layer and internal granule cell layer. Considerable numbers of calbindin-like nerve cells were also found in the olfactory tract and in distal portions of the anterior olfactory nucleus. When comparing the distribution of calbindin-positive structures to that of parvalbumin-positive ones a partially complementary distribution pattern was found. Calbindin-like immunoreactive portions of the anterior olfactory nucleus and olfactory tract were mirrored by immunonegative areas in adjacent sections stained for parvalbumin. Using the combined pigment-Nissl procedure we observed the presence of lipofuscin deposits in nearly 80% of all the calbindin-immunoreactive neurons analysed. Moreover, analysis of their lipofuscin deposits rendered the further differentiation of morphologically similar neuronal subpopulations possible. In contrast, all parvalbumin-like immunoreactive neurons remained free of lipofuscin granules.

Adult↗
PubMed1991

Alzheimer lesions in the entorhinal region and isocortex in Parkinson's and Alzheimer's diseases.

Neuropathologic examination in elderly individuals and patients with Parkinson's disease with and without dementia reveals abundant isocortical amyloid deposits with no or only a few neuritic plaques, neuropil threads (NT), and neurofibrillary tangles (NFT), whereas NT and NFT may be present only in the entorhinal region of the parahippocampal cortex. In Down's syndrome, Alzheimer's disease, and Parkinson's disease, early neuronal degeneration with deposition of NT and NFT may selectively involve layer pre-alpha (II) of the entorhinal region (Brodmann 26 area) forming the origin of the glutamatergic perforant pathway. Its bilateral destruction isolates the hippocampus from isocortical influx. Comparative studies in a series of aged subjects and those with Parkinson's disease show that psychostatus correlates better with the number of NT and NFT in the entorhinal region than in hippocampal area CA-1 and isocortex. This pattern of neuronal degeneration may explain cognitive impairment in early stages of both Alzheimer's and Parkinson's diseases.

Aged↗
PubMed1991

Demonstration of amyloid deposits and neurofibrillary changes in whole brain sections.

Selective and sensitive silver staining of extracellular amyloid deposits and intraneuronal neurofibrillary changes can be applied to 50-150 microns thick polyethylene glycol sections and/or 5-15 microns thick paraffin sections. The silver techniques take advantage of physical development of the nucleation sites thus permitting tight control of the entire procedure. Both techniques can be applied to routinely fixed autopsy material. They do not require particular skills and considerably facilitate processing of large numbers of sections through entire hemispheres of the human brain.

Alzheimer Disease↗
PubMed1991

[Morphological changes in the human cerebral cortex in dementia].

Many diseases of the brain leading to impairment of intellectual capacities are associated with morphological changes in the anteromedial portions of the temporal lobe. Among these are Alzheimer's disease, Parkinson's disease and the syndrome of dementia with argyrophilic grains. The hallmarks of Alzheimer's disease are intraneuronal neurofibrillary changes and extracellular amyloid deposits. The neurofibrillary changes consist of neurofibrillary tangles, neuritic plaques and neuropil threads. The distribution pattern of neurofibrillary changes differs from the distribution of amyloid deposits. The neurofibrillary changes exhibit a distinct but varying distribution pattern in different areas of the cerebral cortex. In fully developed Alzheimer's disease, both the hippocampal formation and isocortical association areas are severely involved while the brunt of the pathology is found in the entorhinal region. The entorhinal region receives information from various isocortical association areas and limbic circuits and projects to the hippocampal formation via the perforant path. This fibre tract is mainly generated by projection neurons within the superficial entorhinal cell layer. In Alzheimer's disease virtually all projection neurons within this layer are destroyed by neurofibrillary tangles. In cases of Parkinson's disease with progressive cognitive decline the neurofibrillary changes are confined to the outer cellular layer of the entorhinal region. In cases of "dementia with argyrophilic grains" the argyrophilic grains are predominantly encountered in the hippocampal formation and in the outer layers of the entorhinal region.(ABSTRACT TRUNCATED AT 250 WORDS)

Alzheimer Disease↗
PubMed1990

[Morphology of Alzheimer disease].

During the course of Alzheimer's disease, considerable amounts of abnormal proteins accumulate within the brain, in particular in the cortex. Some of this material is extracellular (amyloid), some within the neurons (neurofibrillary changes). The extent of the pathological deposits is variable, some regions being particularly severely involved. The entorhinal cortex is already destroyed in the initial phase, followed, in a stepwise fashion, by the hippocampus and the association areas in the isocortex. The undisturbed transfer of information from the isocortical association areas to the hippocampus via the entorhinal area is of importance for mnestic functions. The destructive cortical changes of Alzheimer's disease lead to early and severe impairment or complete blockage of this information pathways.

Aged↗
PubMed1990

Vasopressinergic neurons in the magnocellular nuclei of the human basal forebrain.

Vasopressinergic structures were examined within the magnocellular nuclei of the human basal forebrain. Vasopressinergic neurons were found in all parts of the diagonal band nucleus, and less frequently in the anteromedial subnucleus of the basal nucleus (Meynert). They belong to the group of large multipolar neurons, previously defined as type I neurons, characterized by fine lipofuscin granules widely spread within the soma. Species differences exist in the topographic arrangement of vasopressinergic structures.

Adult↗