Biomedical subjects

H Braak

Publications and source records attributed to H Braak.

At least 19 recordsLinked to original sources

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

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

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

Neurofibrillary changes confined to the entorhinal region and an abundance of cortical amyloid in cases of presenile and senile dementia.

Cases of old-aged demented individuals exhibited abundant cortical amyloid deposits but only small numbers of neurofibrillary changes. Neuritic plaques were rare or absent. Neither Ammon's horn nor isocortex revealed sufficiently large numbers of tangles to permit the diagnosis of fully developed Alzheimer's disease. Dense accumulations of neurofibrillary tangles and neuropil threads occurred only in layer Pre-alpha (II) of the entorhinal region. This pattern of cortical destruction may represent a variant of Alzheimer's disease or an initial stage of this disorder.

Aged↗

PubMed1990

Cognitive impairment in Parkinson's disease: amyloid plaques, neurofibrillary tangles, and neuropil threads in the cerebral cortex.

Sensitive silver methods for extracellular amyloid and intraneuronal cytoskeleton abnormalities (neurofibrillary tangles and neuropil threads) were employed to examine the cortical pathology in Parkinson's disease. In cases with cognitive impairment many plaque-like amyloid deposits were found in the cerebral cortex. Neuritic plaques were rare or absent. Neither the Ammon's horn nor the isocortex revealed a sufficiently large number of tangles to permit the diagnosis of a coexisting fully developed Alzheimer's disease. Large numbers of neurofibrillary tangles and neuropil threads were only found in layer Pre-alpha of the entorhinal cortex. This layer gives rise to major portions of the perforant tract, a pathway which serves as a link in the transmission of data from isocortical association areas to the hippocampal formation. During the course of Parkinson's disease the hippocampal formation is thus endangered to become disrupted from isocortical influences. It is concluded that the cognitive impairment shown by many individuals suffering from Parkinson's disease may partly be caused by cortical lesions.

Aged↗

PubMed1990

Alzheimer's disease: striatal amyloid deposits and neurofibrillary changes.

Sensitive silver methods were employed for the examination of extracellular amyloid and intraneuronal neurofibrillary changes in the striatum of Alzheimer's disease patients. Numerous amyloid deposits were present in the striatum whereas neuritic (senile) plaques were only rarely encountered. Many large and a few medium-sized nerve cells had neurofibrillary tangles within their somata and according to morphological criteria corresponded to local circuit neurons. Numerous argyrophilic threads in the neuropil were scattered throughout the nuclear gray matter. The striatum of non-demented individuals was virtually devoid of amyloid and neurofibrillary changes.

Adult↗

PubMed1989

Alzheimer's disease: mismatch between amyloid plaques and neuritic plaques.

Isocortical amyloid deposits and neurofibrillary changes were studied using selective silver staining methods. Amyloid was found in plaque-like formations varying in size and shape. The distribution pattern of these plaques as seen in the silver-stained preparations was identical to that recognized by A4 protein (amyloid) immunostaining. Consecutive sections stained for amyloid and neurofibrillary changes revealed the absence of intraneuronal cytoskeleton abnormalities within the boundaries of many of the amyloid plaques. Congo red preparations did not show these plaques and the tissue within the range of the plaques did not reveal any conspicuous neuropil distortions and/or glial cell accumulations. Hence, a considerable proportion of the amyloid plaques do not correspond to and should carefully be distinguished from 'primitive', 'mature', and 'burned out' types of neuritic (senile) plaques.

Aged↗

PubMed1989

The presubicular region in Alzheimer's disease: topography of amyloid deposits and neurofibrillary changes.

Specific silver impregnation techniques for extracellular amyloid and intraneuronal neurofibrillary changes were used to examine the presubiculum in Alzheimer victims. Extended amyloid clouds in the absence of neurofibrillary changes were noted in the parvopyramidal layer of the presubiculum proper. The corresponding layer in the parasubiculum, in contrast, showed many neurofibrillary tangles and neuropil threads in the absence of amyloid. The transsubicular parvopyramidal layer contained both amyloid deposits and neurofibrillary changes. This severe involvement of all subdivisions of the presubicular region in Alzheimer's disease is considered to impair functions of the Papez circuit.

Alzheimer Disease↗

PubMed1989

Auditory brainstem nuclei in Alzheimer's disease.

Serial sections of 7 Alzheimer brainstems were examined. The histopathological hallmarks were demonstrated by means of Kongo red- and silver-stained preparations. A subsequent counterstaining with a Nissl dye, allowing the cytoarchitectonical interpretation, revealed a considerable plaque formation in the central nucleus and the dorsomedial nucleus of the inferior colliculus. To a lesser degree plaques were also present in the deep layers of the dorsal cortex of the inferior colliculus. All other auditory brainstem nuclei were devoid of neuritic plaques. Neurofibrillary tangles were rarely seen. They occur in the dorsal cochlear nucleus, the periolivary region, the ventral nucleus of the lateral lemniscus, and in the central nucleus of the inferior colliculus.

Alzheimer Disease↗

PubMed1989

The human oral raphe system. Architectonics and neuronal types in pigment-Nissl preparations.

Serial sections (15 microns, 120 microns, and 400 microns) of nine brain stems treated with a combined lipofuscin pigment-Nissl stain were examined in order to delineate the three-dimensional conformation and subdivisions as well as the neuronal types of the human oral raphe system. Characteristic lipofuscin deposits within the somata of various cell types facilitated the demarcation of the oral raphe nuclei from surrounding structures. The dorsal, central, and linear raphe nuclei, e.g. the major subdivisions of the oral raphe system, share common traits as far as neuronal composition and pigmentation is concerned. The interfascicular subnucleus, the dorsofascicular subnucleus, and the intercalate subnucleus are minor subdivisions of the dorsal raphe nucleus. The intercalate one cannot be differentiated from surrounding areas in preparations solely stained for Nissl-material, while it can facilely be identified in combined pigment-Nissl preparations by virtue of differences in the pigmentation pattern. Our architectonical concept of the oral raphe system is in good accordance with the one derived from immunocytochemical investigations of serotonin-containing neurons in the human brain stem. Furthermore, five main neuronal types are described which constitute the oral raphe nuclei. They have been differentiated according to their characteristics as seen in combined pigment-Nissl preparations. I) Large ovoid to polygonal neurons with densely packed and intensely stained pigment granules. II) Similarly featured cells displaying dust-fine and faintly stained pigment granules. III) Medium-sized, ovoid to polygonal neurons with loosely distributed, small pigment granules. IV) Small ovoid neurons devoid of pigment or with only few, intensely stained granules. V) Small spindle-shaped nerve cells with various amounts of intensely stained pigment granules.(ABSTRACT TRUNCATED AT 250 WORDS)

Autopsy↗