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PubMed1983

Pathological changes in the nucleus of Meynert in Alzheimer's and Parkinson's diseases.

Combined neuropathological and neurochemical assessment of the nucleus of Meynert in senile dementia of Alzheimer type (SDAT) have demonstrated that the cholinergic biochemical activity, choline acetyltransferase, is more extensively reduced in the nucleus (over 90%) than the loss of putative cholinergic perikarya (35%). Acetylcholinesterase histochemical activity was however substantially retained in individual neurones in the nucleus although virtually absent from the neocortex in SDAT. These abnormalities are consistent with a primary degeneration of cholinergic axons projecting to the cortex and secondary loss of perikarya from the subcortical nucleus. In contrast, preliminary observations on cases of Parkinson's disease suggest that the neuronal loss from the nucleus of Meynert may be greater in this disease than in SDAT, and previous studies have not consistently demonstrated a reduction in cortical choline acetyltransferase activities in Parkinson's disease. These observations, together with major differences in the neuropathology of the nucleus in SDAT and Parkinson's disease (neurofibrillary tangle and Lewy body formation, respectively) suggest that the involvement of the cholinergic system may differ in the two disease processes.

Acetylcholinesterase↗
PubMed1984

Chromatographic characterization of neuropeptides in post mortem human brain.

Reverse phase high performance liquid chromatography was used to establish the immunoreactive species of five neuropeptides (thyrotropin-releasing hormone, luteinising hormone-releasing hormone, neurotensin, substance-P and somatostatin) in three areas of post mortem human brain--the hypothalamus, amygdala and cortex. In the majority of cases the major immunoreactive peak corresponded to the authentic peptide, although other peaks of immunoreactivity were observed in several instances. It was established that somatostatin-14 was present as the major immunoreactive form and that somatostatin-28 did not occur in any of the three brain areas, although other somatostatin-immunoreactive peaks of unknown structure were detected. In addition to authentic neurotensin in the cortex, a substantial peak of immunoreactivity corresponding to the elution time of neurotensin (1-11) was observed. LH-RH was not detected in the amygdala, but was present in the cortex as a minor component of overall immunoreactivity. The major peak of substance-P immunoreactivity in all three brain areas corresponded to authentic substance-P; in addition immunoreactive material eluting in the region of [Met-O] substance-P, substance-P (5-11) and substance-P (6-11) were detected. TRH occurred as the major peak in all three areas, although minor peaks of immunoreactivity were seen in the amygdala.

Adult↗
PubMed1985

Somatostatin immunoreactivity in cortical and some subcortical regions in Alzheimer's disease.

Reverse phase HPLC analysis of somatostatin immunoreactivity in the cerebral cortex in elderly normal individuals revealed that the majority of the immunoreactivity co-eluted with synthetic somatostatin-14. While an immunoreactive peak corresponding to somatostatin-28 was not detected there was a peak of immunoreactivity which eluted after somatostatin-14. In cases of senile dementia of Alzheimer type (SDAT), where abundant neurofibrillary tangles and senile plaques (density greater than 30 per 1.3-mm2 field) were present in the cerebral cortex, somatostatin immunoreactivity was found to be significantly decreased in either the frontal or temporal cortex. Chromatographic analysis, however, revealed that both the major immunoreactive peaks detected in the normal group were reduced in SDAT in the temporal and frontal cortex. Using a punch microdissection technique somatostatin immunoreactivity has been assessed in the nucleus of Meynert and amygdala of SDAT and elderly normal cases. While there was no change in somatostatin immunoreactivity in the nucleus of Meynert in the SDAT group, tissue punches taken from the amygdala revealed a selective decrease in somatostatin immunoreactivity in the basal nucleus, in the SDAT cases.

Aged↗
PubMed1986

Cerebellar structure and function in the murine mutant "jolting".

The morphology of the cerebellar cortex of the murine mutant "jolting" and its phenotypically normal littermate was studied. The general organisation of the cerebellum of normal mice was similar in all respects to that described for other vertebrate species. In "jolting" mice aged 4 months or more there was a marked loss of Purkinje cells and spheroids were present on Purkinje cell axons. An ultrastructural examination showed that the spheroids contained randomly orientated neurofilaments, degenerating mitochondria and autophagic vacuoles. The abnormalities in the cerebellum appeared confined to the Purkinje cells. Extracellular recordings were made of the electrical activity of the cerebellar cortex of anaesthetised mice. In the cerebellar cortex of "jolting" animals, Purkinje cells generated little spontaneous activity, but complex discharges resulting from climbing fibre inputs were indistinguishable from normal. The abnormal electrical activity of Purkinje cells in "jolting" mice could be seen in animals as young as 3 weeks. It was concluded that the "jolting" mouse suffers from a cerebellar ataxia.

Action Potentials↗
PubMed1987

Serum creatine kinase-BB levels and cerebral cortical creatine kinase activity in senile dementia of the Alzheimer type.

A rise in serum creatine kinase-BB (CK-BB) levels has been reported previously in cases of dementia. In the present study the levels of serum CK-BB have been measured in patients clinically assessed to have senile dementia of the Alzheimer's type (SDAT) and in cognitively intact individuals, matched for age, by a specific two-site monoclonal immunoradiometric assay. No significant difference was found between the 2 groups. Total creatine kinase activity in temporal cortex (Brodmann area 21 and 22) was also found to be similar in brains from SDAT or control cases, obtained at autopsy. These results suggest no major change in the permeability of the blood-brain barrier to this enzyme in SDAT patients.

Alzheimer Disease↗
PubMed1988

Cortical somatostatinergic system not affected in Alzheimer's and Parkinson's diseases.

A reduction in the levels of somatostatin-like immunoreactivity (SLI) and somatostatin binding sites in the cerebral cortex has been previously reported to occur in Alzheimer's disease (AD) and Parkinson's disease with associated dementia. In the present study, the levels of both SLI and high affinity [3H]somatostatin binding sites have been measured in the frontal (Brodmann area 9) and temporal (Brodmann area 21) cortices in patients with presenile and senile Alzheimer's disease, and in mentally normal and cognitively impaired cases of Parkinson's disease. The results were compared with those obtained from a group of normal patients matched for age and postmortem delay. No significant changes in SLI or somatostatin binding in the frontal and temporal cortex were found between any of the disease groups. These results suggest that involvement of the somatostatinergic system in AD or Parkinson's disease is not a consistent or primary neurochemical feature of these diseases.

Adult↗
PubMed1989

Comparison of the regional distribution of transferrin receptors and aluminium in the forebrain of chronic renal dialysis patients.

Recent studies have emphasised the potential neurotoxicity of aluminium in dialysis encephalopathy and it has also been suggested that this element may have a role in the pathogenesis of Alzheimer's disease. Aluminium is known to be transported by the iron transport protein transferrin. In this study using receptor autoradiography we have demonstrated the presence of transferrin binding sites in the human forebrain and shown a pattern similar to that found in other species. Imaging secondary ion mass spectrometry has demonstrated the distribution of aluminium-containing cell-like profiles in the brains of chronic renal dialysis patients who have raised levels of brain aluminium (greater than 4 micrograms/g dry weight) and even in dialysis patients where the gross level of aluminium was within the normal range. The density of these profiles corresponded to the regions of high transferrin receptor density. In contrast, the distribution of iron in the brain showed an inverse correlation with transferrin receptor density with highest iron levels present in the globus pallidus, an area of low transferrin receptor density. These results suggest that the regional distribution of neuropathological changes seen in dialysis encephalopathy patients and also Alzheimer's disease may reflect the distribution of transferrin receptors. The discrepancy between iron distribution and transferrin receptor distribution suggests that further, as yet uncharacterized mechanisms, govern the distribution of brain iron.

Adult↗
PubMed1990

Parameters of cholinergic neurotransmission in the thalamus in Parkinson's disease and Alzheimer's disease.

Loss of cholinergic cells in the basal forebrain is associated with commensurate reductions in cortical acetylcholine-related enzyme activities in both Alzheimer's disease (AD) and Parkinson's disease (PD). Nerve cell loss from the cholinergic pontine tegmental nuclei also occurs. As the latter nuclei project to the diencephalon, we used frozen tissue from 5 controls, 5 PD and 5 AD cases to study the distribution of ChAT, AChE and [3H]nicotine binding in the thalamus and subthalamic nucleus. The anterior nuclear group and the mediodorsal nucleus showed high activities of ChAT and AChE together with relatively high levels of [3H]nicotine binding. The centromedian nucleus and subthalamic nucleus contained equally high levels of ChAT but negligible levels of [3H]nicotine binding. There were no significant changes in the levels of ChAT, AChE and nicotine binding in the PD and AD groups indicating that involvement of the pedunculopontine tegmental nucleus is likely to be a secondary retrograde phenomenon rather than part of a systematic cholinergic fibre degeneration.

Acetylcholine↗
PubMed1992

Distribution of transferrin receptors in relation to cytochrome oxidase activity in the human spinal cord, lower brainstem and cerebellum.

Neuronal activity and oxidative energy metabolism are tightly coupled. There is evidence that cytochrome oxidase, the terminal enzyme of the electron transport chain, can serve as a metabolic marker of neuronal activity. All the respiratory chain enzymes have iron containing prosthetic groups and therefore represent an important component of iron utilisation. Since iron entry into cells is mediated by the transferrin receptor, this receptor may also serve as marker of neuronal activity. The histochemical distribution of cytochrome oxidase has therefore been compared with the autoradiographic distribution of the transferrin receptor in the human spinal cord, brainstem and cerebellum. Cytochrome oxidase activity showed a very similar pattern of distribution to the transferrin receptor in the spinal cord, brainstem and cerebellum. The highest levels of cytochrome oxidase activity and transferrin receptor binding were associated with; in the spinal cord, the substantia gelatinosa, laminae II and III and the motor neurones; in the medulla and pons, the spinal trigeminal nucleus, hypoglossal nucleus, dorsal motor nucleus of the vagus, inferior and superior olives, nucleus praepositus, nucleus paramedianus, central grey, superior central nuclei and locus coeruleus; in the cerebellum, the molecular layer. The results suggest that the transferrin receptor may provide a useful marker of total neuronal respiratory activity.

Aged↗
PubMed1992

Aluminium accumulation in relation to senile plaque and neurofibrillary tangle formation in the brains of patients with renal failure.

The effects of long-term exposure to aluminium on the development of Alzheimer-type neuropathological changes have been studied post-mortem in patients with chronic renal failure who did not have dialysis encephalopathy. Administration of aluminium-containing phosphate binding compounds appears to be a major factor in the accumulation of aluminium in the brain of dialysis patients. The mean serum aluminium concentrations determined during life and brain aluminium concentrations determined post-mortem correlated with both the duration and total amount of aluminium hydroxide administered to these patients. No correlation was found between the presence of bone aluminium and either the mean serum or brain aluminium concentration. Longitudinal monitoring of serum aluminium concentrations may provide a more reliable index than bone biopsy of brain aluminium concentrations in dialysis patients. Dynamic secondary ion mass spectrometry revealed focal accumulations of aluminium associated with cortical pyramidal neurones. The majority of patients also showed immunostaining in pyramidal neurones with an antibody to the N-terminal region of the beta/A4 amyloid precursor protein, while staining was absent in age-matched control cases. One-third of the patients exhibited beta/A4-positive amorphous senile plaques in the cerebral cortex. However, there was no clear correlation between either the presence and intensity of beta/A4 amyloid precursor immunostaining or the presence of senile plaques and the concentration of aluminium in the cerebral cortex. Cortical neurofibrillary tangles were not observed in any of the dialysis patients. These data suggest that it is unlikely that aluminium plays any major role in neurofibrillary tangle formation and that its putative role in senile plaque formation is likely to be only part of a complex cascade of changes.

Aluminum↗