Diagenetic processes in ore formation with special reference to the Zambian copperbelt and permian marl slate.

This thesis is concerned with the role of diagenesis in forming ore deposits. Two sedimentary 'ore-types' have been examined; the Proterozoic copper-cobalt orebodies of the Konkola Basin on the Zambian Copperbelt, and the Permian Marl Slate of North East England. Facies analysis of the Konkola Basin shows the Ore-Shale to have formed in a subtidal to intertidal environment. A sequence of diagenetic events is outlined from which it is concluded that the sulphide ores are an integral part of the diagenetic process. Sulphur isotope data establish that the sulphides formed as a consequence of the bacterial reduction of sulphate, while the isotopic and geochemical composition of carbonates is shown to reflect changes in the compositions of diagenetic pore fluids. Geochemical studies indicate that the copper and cobalt bearing mineralising fluids probably had different sources. Veins which crosscut the orebodies contain hydrocarbon inclusions, and are shown to be of late diagenetic lateral secretion origin. RbiSr dating indicates that the Ore-Shale was subject to metamorphism at 529 A- 20 myrs. The sedimentology and petrology of the Marl Slate are described. Textural and geochemical studies suggest that much of the pyrite (framboidal) in the Marl Slate formed in an anoxic water column, while euhedral pyrite and base metal sulphides formed within the sediment during early diagenesis. Sulphur isotope data confirm that conditions were almost "ideal" for sulphide formation during Marl Slate deposition, the limiting factors in ore formation being the restricted supply of chalcophile elements. Carbon and oxygen isotope data, along with petrographic observations, indicate that much of the calcite and dolomite occurring in the Marl Slate is primary, and probably formed in isotopic equilibrium. A depositional model is proposed which explains all of the data presented and links the lithological variations with fluctuations in the anoxicioxic boundary layer of the water column.

Genetic studies of Cu-Pb-Zn mineralisation in Triassic red beds of Western Europe

Continental red bed sequences are host, on a worldwide scale, to a characteristic style of mineralisation which is dominated by copper, lead, zinc, uranium and vanadium. This study examines the features of sediment-hosted ore deposits in the Permo-Triassic basins of Western Europe, with particular reference to the Cu-Pb-Zn-Ba mineralisation in the Cheshire Basin, northwest England, the Pb-Ba-F deposits of the Inner Moray Firth Basin, northeast Scotland, and the Pb-rich deposits of the Eifel and Oberpfalz regions, West Germany. The deposits occur primarily but not exclusively in fluvial and aeolian sandstones on the margins of deep, avolcanic sedimentary basins containing red beds, evaporites and occasionally hydrocarbons. The host sediments range in age from Permian to Rhaetian and often contain (or can be inferred to have originally contained) organic matter. Textural studies have shown that early diagenetic quartz overgrowths precede the main episode of sulphide deposition. Fluid inclusion and sulphur isotope data have significantly constrained the genetic hypotheses for the mineralisation and a model involving the expulsion of diagenetic fluids and basinal brines up the faulted margins of sedimentary basins is favoured. Consideration of the development of these sedimentary basins suggests that ore emplacement occurred during the tectonic stage of basin evolution or during basin inversion in the Tertiary. ð34S values for barite in the Cheshire Basin range from 13.8% to 19.3% and support the theory that the Upper Triassic evaporites were the principal sulphur source for the mineralisation and provided the means by which mineralising fluids became saline. In contrast, δ34S values for barite in the Inner Moray Firth Basin (mean δ34S = + 29%) are not consistent with simple derivation of sulphur from the evaporite horizons in the basin and it is likely that sulphur-rich Jurassic shales supplied the sulphur for the mineralisation at Elgin. Possible sources of sulphur for the mineralisation in West Germany include hydrothermal vein sulphides in the underlying Devonian sediments and evaporites in the overlying Muschelkalk. Textural studies of the deeply buried sandstones in the Cheshire Basin reveal widespread dissolution and replacement of detrital phases and support the theory that red bed diagenetic processes are responsible for the release of metals into pore fluids. The ore solutions are envisaged as being warm (60-150%C), saline (9-22 wt % equiv NaCl) fluids in which metals were transported as chloride complexes. The distribution of δ34S values for sulphides in the Cheshire Basin (-1.8% to + 16%), the Moray Firth Basin (-4.8% to + 27%) and the German Permo-Triassic Basins (-22.2% to -12.2%) preclude a magmatic source for the sulphides and support the contention that sulphide precipitation is thought to result principally from sulphate reduction processes, although a decrease in temperature of the ore fluid or reaction with carbonates may also be important. Methane is invoked as the principal reducing agent in the Cheshire Basin, whilst terrestrial organic debris and bacterial reduction processes are thought to have played a major part in the genesis of the German ore deposits.

Palaeozoic volcanogenic mineral deposits at Parys Mountain, Avoca, and S.E. Canada: a comparative study. Available in 2 volumes.

The sulphide mineralisation at Avoca and Parys Mountain is intimately related to volcanism and is of volcanogenic sedimentary type. The associated volcanics are predominantly pyroclastics of rhyodacitic composition and of Upper Ordovician age. They were erupted from discrete small volcanic centres, products of single local volcanic events, whose spatial distribution was related to fractures in the sialic basement of the paratectonic Caledonides of the British Isles. These fractures resulted in linear controls on volcanic, plutonic and tectonic features; they are the result of predominantly strikeslip stresses generated in this part of the European plate during closure of the Iapetus ocean. The mineralisation, predominantly pyritic, consists of a siliceous footwall zone containing bedded and cross-cutting sulphides and an overlying non-siliceous zone of bedded sulphides which may show vertical zoning of metal ratios. The sulphides are associated with chert and iron formation and have been affected by slumping. Mineralisation developed near the vents during intense fumarolic activity accompanying strong volcanism; at Parys Mountain, fumarolic activity commenced prior to, and continued after, the rnain volcanic event. Comparison with similar deposits in Newfoundland and at Bathurst, in the Canadian Appalachians, shows that mineralisation can be associated with any discrete pulse of acid magmatism in shallow subaqueous conditions. Local features of the sulphides and associated sediments are similar, although in more distal deposits (with respect to a volcanic centre) footwall alteration and mineralisation are less well developed. The nature of the basement and the presence or absence of earlier volcanics are not critical, although establishment of a local tensional regime at the time of ore formation may be important. The volcanics hosting mineralisation are rhyodacitic pyroclastics, generally related to a small centre and representing a single episode of volcanism.

Spatial correlations between beta-amyloid (Abeta) deposits and blood vessels in early-onset Alzheimer's disease

In cases of late-onset Alzheimer’s disease (AD), there is a spatial correlation between the classsic ‘cored’ type of Beta-amyloid (Abeta) deposit and the large vertically penetrating arterioles in the cerebral cortex suggesting that blood vessels are involved in the pathogenesis of the classic deposits. In this chapter, the spatial correlations between the diffuse, primitive, and classic Abeta deposits and blood vessels were studied in 10 cases of early-onset AD in the age range 40 – 65 years. Sections of frontal cortex were immunostained with antibodies against Abeta?and with collagen IV to reveal the Abeta deposits and blood vessel profiles. In the early-onset cases as a whole, all types of Abeta? deposit and blood vessel profiles were distributed in clusters. There was a positive spatial correlation between the clusters of the diffuse Abeta deposits and the larger (>10µm) and smaller diameter (<10?m) blood vessel profiles in one and three cases respectively. The primitive and classic Abeta deposits were spatially correlated with larger and smaller blood vessels both in three and four cases respectively. Spatial correlations between the Abeta deposits and blood vessels may be more prevalent in cases expressing amyloid precursor protein (APP) than presenilin 1 (PSEN1) mutations. Apolipoprotein E (Apo E) genotype of the patient did not appear to influence the spatial correlation with blood vessel profiles. The data suggest that the larger diameter blood vessels are less important in the pathogenesis of the classic Abeta deposits in early-onset compared with late-onset AD.

The spatial patterns of beta-amyloid (Abeta) deposits and neurofibrillary tangles (NFT) in late-onset sporadic Alzheimer's disease

The spatial patterns of beta-amyloid (Abeta) deposits and neurofibrillary tangles (NFT) were studied in areas of the cerebral cortex in 16 patients with the late-onset, sporadic form of Alzheimer’s disease (AD). Diffuse, primitive, and classic Abeta deposits and NFT were aggregated into clusters; the clusters being regularly distributed parallel to the pia mater in many areas. In a significant proportion of regions, the sizes of the regularly distributed clusters approximated to those of the cells of origin of the cortico-cortical projections. The diffuse and primitive Abeta deposits exhibited a similar range of spatial patterns but the classic Abeta deposits occurred less frequently in large clusters >6400microm. In addition, the NFT often occurred in larger regularly distributed clusters than the Abeta deposits. The location, size, and distribution of the clusters of Abeta deposits and NFT supports the hypothesis that AD is a 'disconnection syndrome' in which degeneration of specific cortico-cortical and cortico-hippocampal pathways results in synaptic disconnection and the formation of clusters of NFT and Abeta deposits.

Spatial correlations between the vacuolation, prion protein (PrPsc) deposits and the cerebral blood vessels in sporadic Creutzfeldt-Jakob disease

In the variant form of Creutzfeldt-Jakob disease (vCJD), 'florid' deposits of the protease resistant form of prion protein (PrP(sc)) were aggregated around the cerebral blood vessels suggesting the possibility that prions may spread into the brain via the cerebral microcirculation. The objective of the present study was to determine whether the pathology was spatially related to blood vessels in cases of sporadic CJD (sCJD), a disease without an iatrogenic etiology, and therefore, less likely to be caused by hematogenous spread. Hence, the spatial correlations between the vacuolation ('spongiform change'), PrP(sc) deposits, and the blood vessels were studied in immunolabelled sections of the cerebral cortex and cerebellum in eleven cases of the common M/M1 subtype of sCJD. Both the vacuolation and the PrP(sc) deposits were spatially correlated with the blood vessels; the PrP(sc) deposits being more focally distributed around the vessels than the vacuoles. The frequency of positive spatial correlations was similar in the different gyri of the cerebral cortex, in the upper and lower cortical laminae, and in the molecular layer of the cerebellum. It is hypothesized that the spatial correlation is attributable to factors associated with the blood vessels which promote the aggregation of PrP(sc) to form deposits rather than representing the hematogenous spread of the disease. The aggregated form of PrP(sc) then enhances cell death and may encourages the development of vacuolation in the vicinity of the blood vessels.

Size frequency distribution of the β-amyloid (aβ) deposits in dementia with Lewy bodies with associated Alzheimer’s disease pathology

The objective is to study beta-amyloid (Abeta) deposition in dementia with Lewy bodies (DLB) with Alzheimer's disease (AD) pathology (DLB/AD). The size frequency distributions of the Abeta deposits were studied and fitted by log-normal and power-law models. Patients were ten clinically and pathologically diagnosed DLB/AD cases. Size distributions had a single peak and were positively skewed and similar to those described in AD and Down's syndrome. Size distributions had smaller means in DLB/AD than in AD. Log-normal and power-law models were fitted to the size distributions of the classic and diffuse deposits, respectively. Size distributions of Abeta deposits were similar in DLB/AD and AD. Size distributions of the diffuse deposits were fitted by a power-law model suggesting that aggregation/disaggregation of Abeta was the predominant factor, whereas the classic deposits were fitted by a log-normal distribution suggesting that surface diffusion was important in the pathogenesis of the classic deposits.

Laminar distribution of β-amyloid deposits in dementia with Lewy bodies and in Alzheimer's disease

This study tested whether the laminar distribution of the β-amyloid (Aβ) deposits in dementia with Lewy bodies (DLB) cases with significant Alzheimer's disease (AD) pathology (DLB/AD) was similar to "pure" AD. In DLB/AD, the maximum density of the diffuse and primitive deposits occurred either in the upper laminae or a bimodal distribution was present with density peaks in the upper and lower laminae. A bimodal distribution of the classic Aβ deposits was also observed. Compared with AD, DLB/AD cases had fewer primitive deposits relative to the diffuse and classic deposits; the primitive deposits exhibited a bimodal distribution more frequently, and the diffuse deposits occurred more often in the upper laminae. These results suggest that Aβ pathology in DLB/AD may not simply represent the presence of associated AD. © 2006 Sage Publications.

Spatial correlations between the vacuolation, prion protein deposits, and surviving neurons in the cerebral cortex in sporadic Creutzfeldt-Jakob disease

In the cerebral cortex of cases of sporadic Creutzfeldt-Jakob disease (sCJD), the vacuolation (spongiform change) and PrP deposits are aggregated into clusters which are regularly distributed parallel to the pia mater. The objective of the present study was to determine the spatial relationships between the clusters of the vacuoles and PrP deposits and between the pathological changes and variations in the density of surviving neurons. In areas with low densities of pathological change, clusters of vacuoles were spatially correlated with the surviving neurons and not with the PrP deposits. By contrast, in more significantly affected areas, clusters of vacuoles were spatially correlated with those of the PrP deposits and not with the surviving neurons. In addition, areas with a high density of vacuoles and a low density of PrP deposits exhibited no spatial correlations between the variables. These data suggest that the spatial relationships between the vacuolation, PrP deposits and surviving neurons in sCJD depend on the density of lesions present. Differences in the pattern of correlation may reflect the developmental stage of the pathology in particular cortical areas.

The distribution of senile plaques, neurofibrillary tangles and beta/A4 deposits in the hippocampus in Alzheimer's disease

The density of senile plaques (SP) and neurofibrillary tangles (NFT) was studied in Glees and Marsland stained sections of the hippocampus and parahippocampal gyrus (PHG) in 20 pateints with Alzheimer's disease. In addition, in six of the patients, the density of beta/A4 protein deposits, as revealed by immunohistochemistry and neurofibrillary changes demonstrated with the Gallyas stain, were studied in adjacent sections. The density of Glees SP and beta/A4 deposits was significantly greater in area CA1 of the hippocampus and in the subiculum than in the PHG. Hence, neurofibrillary degeneration appears to be a more important lesion than beta/A4 deposition in the hippocampus compared with the PHG. In addition, the detailed distribution of the lesions in the hippocampus could be explained if beta/A4/SP and NFT occur on the axon terminals and in the cell bodies respectively of the same neurons.

Spatial correlations between beta-amyloid (A beta) deposits and blood vessels in familial Alzheimer's disease

In sporadic Alzheimer’s disease (SAD), the classic (‘dense-cored’) ß-amyloid (Aß) deposits are aggregated around the larger blood vessels in the upper laminae of the cerebral cortex. To determine whether a similar relationship exists in familial AD (FAD), the spatial correlations between the diffuse, primitive, and classic ß-amyloid (Aß deposits and blood vessels were studied in ten FAD cases including cases linked to amyloid precursor protein (APP) and presenilin (PSEN) gene mutations and expressing apolipoprotein E (apo E) allele E4. Sections of frontal cortex were immunolabelled with antibodies against Aß and with collagen IV to reveal the Aß deposits and blood vessel profiles. In the FAD cases as a whole, Aßdeposits were distributed in clusters. There was a positive spatial correlation between the clusters of the diffuse Aßdeposits and the larger (>10 µm) and smaller diameter (<10 µm) blood vessels in one and three cases respectively. The primitive Aß deposits were spatially correlated with larger and smaller blood vessels each in four cases and the classic deposits in three and four cases respectively. Apo E genotype of the patient did not influence spatial correlation with blood vessels. Hence, spatial correlations between the classic deposits and larger diameter blood vessels were significantly less frequent in FAD compared with SAD. It was concluded that both Aß deposit morphology and AD subtype determine spatial correlations with blood vessels in AD.

Size frequency distributions of abnormal protein deposits in Alzheimer’s disease and variant Creutzfeldt-Jakob disease

TThe size frequency distributions of ß-amyloid (Aß) and prion protein (PrPsc) deposits were studied in Alzheimer’s disease (AD) and the variant form of Creutzfeldt-Jakob disease (vCJD) respectively. All size distributions were unimodal and positively skewed. Aß deposits reached a greater maximum size and their distributions were significantly less skewed than the PrPsc deposits. All distributions were approximately log-normal in shape but only the diffuse PrPsc deposits did not deviate significantly from a log-normal model. There were fewer larger classic Aß deposits than predicted and the florid PrPsc deposits occupied a more restricted size range than predicted by a log-normal model. Hence, Aß deposits exhibit greater growth than the corresponding PrPsc deposits. Surface diffusion may be particularly important in determining the growth of the diffuse PrPsc deposits. In addition, there are factors limiting the maximum size of the Aß and florid PrPsc deposits.

Classic beta-amyloid deposits cluster around large diameter blood vessels rather than capillaries in sporadic Alzheimer's disease

Various hypotheses could explain the relationship between beta-amyloid (Abeta) deposition and the vasculature in Alzheimer's disease (AD). Amyloid deposition may reduce capillary density, affect endothelial cells of blood vessels, result in diffusion from blood vessels, or interfere with the perivascular clearance mechanism. Hence, the spatial pattern of the classic ('cored') type of Abeta deposit was studied in the upper laminae (I,II/III) of the superior frontal gyrus in nine cases of sporadic AD (SAD). Sections were immunostained with antibodies against Abeta and with collagen IV to study the relationships between the spatial distribution of the classic deposits and the blood vessel profiles. Both the classic deposits and blood vessel profiles were distributed in clusters. In all cases, there was a positive spatial correlation between the clusters of the classic deposits and the larger diameter (>10 microm) blood vessel profiles and especially the vertically penetrating arterioles. In only 1 case, was there a significant spatial correlation between the clusters of the classic deposits and the smaller diameter (<10 microm) capillaries. There were no negative correlations between the density of Abeta deposits and the smaller diameter capillaries. In 9/11 cases, the clusters of the classic deposits were significantly larger than those of the clusters of the larger blood vessel profiles. In addition, the density of the classic deposits declined as a negative exponential function with distance from a vertically penetrating arteriole. These results suggest that the classic Abeta deposits cluster around the larger blood vessels in the upper laminae of the frontal cortex. This aggregation could result from diffusion of proteins from blood vessels or from overloading the system of perivascular clearance from the brain.

The spatial patterns of prion protein deposits in cases of variant Creutzfeldt-Jakob disease

The spatial patterns of the prion protein (PrP) deposits were studied in immunostained sections of areas of the cerebral cortex, hippocampus, dentate gyrus, and the molecular layer of the cerebellum in 11 cases of variant Creutzfeldt-Jakob disease (vCJD). Clustering of PrP deposits, with a regular distribution of the clusters parallel to the tissue boundary, was the most common spatial pattern observed. Two morphological types of PrP deposit were recognised, those consisting of a condensed core (florid deposits) and those deposits lacking a condensed core (non-florid deposits). The florid and non-florid PrP deposits exhibited a different profile of spatial patterns. First, the florid deposits exhibited a regularly distributed pattern of clusters more frequently than the non-florid deposits. Second, the florid deposits formed larger clusters (greater than1,600 µm in diameter) less frequently than the non-florid deposits. In the areas of the cerebral cortex that exhibited a regular distribution of PrP deposit clusters, the cluster size of the deposits approximated that of the groups of cells of the cortico-cortical pathway origin in only 12% of analyses. No significant differences in the frequency of the different types of spatial pattern were observed in different brain regions, or in the cerebral cortex between the upper and lower laminae. It was concluded that the spatial patterns of the PrP deposits in the cerebral cortex in vCJD are unlikely to reflect the degeneration of the cortico-cortical pathways as has been reported in sporadic CJD (sCJD). In addition, different factors could be involved in the development of the deposits with and without a condensed core.

Spatial pattern of prion protein deposits in patients with sporadic Creutzfeldt–Jakob disease

The spatial pattern of the prion protein (PrP) deposits was studied in the cerebral cortex and cerebellum in 10 patients with sporadic Creutzfeldt–Jakob disease (CJD). In all patients the PrP deposits were aggregated into clusters and, in 90% of cortical areas and in 50% of cerebellar sections, the clusters exhibited a regular periodicity parallel to the tissue boundary; a spatial pattern also exhibited by ß-amyloid (Aß) deposits in Alzheimer's disease (AD). In the cerebral cortex, the incidence of regular clustering of the PrP deposits was similar in the upper and lower cortical laminae. The sizes of the PrP clusters in the upper and lower cortex were uncorrelated. No significant differences in mean cluster size of the PrP deposits were observed between brain regions. The size, location and distribution of the PrP deposit clusters suggest that PrP deposition occurs in relation to specific anatomical pathways and supports the hypothesis that prion pathology spreads through the brain via such pathways. In addition, the data suggest that there are similarities in the pathogenesis of extracellular protein deposits in prion disease and in AD.