Some studies have found significant concentrations of aluminum in the brains
of PD patients. The following are some abstracts.
 
 
Authors
  Leveugle B.  Spik G.  Perl DP.  Bouras C.  Fillit HM.  Hof PR.
Institution
  Department of Geriatrics and Adult Development, Mount Sinai School of
  Medicine, New York, NY 10029.
Title
  The iron-binding protein lactotransferrin is present in pathologic lesions
  in a variety of neurodegenerative disorders: a comparative
  immunohistochemical analysis.
Source
  Brain Research.  650(1):20-31, 1994 Jul 4.
Abstract
  Lactotransferrin is a glycoprotein that specifically binds and transports
  iron. This protein is also believed to transport other metals such as
  aluminum. Several lines of evidence indicate that iron and aluminum are
  involved in the pathogenesis of many dementing diseases. In this context,
  the analysis of the iron-binding protein distribution in the brains of
  patients affected by neurodegenerative disorders is of particular
  interest. In the present study, the distribution of lactotransferrin was
  analyzed by immunohistochemistry in the cerebral cortex from patients
  presenting with Alzheimer's disease, Down syndrome, amyotrophic lateral
  sclerosis/parkinsonism-dementia complex of Guam, sporadic amyotrophic
  lateral sclerosis, or Pick's disease. The results show that
  lactotransferrin accumulates in the characteristic lesions of the
  different pathologic conditions investigated. For instance, in Alzheimer's
  disease and Guamanian cases, a subpopulation of neurofibrillary tangles
  was intensely labeled in the hippocampal formation and inferior temporal
  cortex. Senile plaques and Pick bodies were also consistently labeled.
  These staining patterns were comparable to those obtained with antibodies
  to the microtubule-associated protein tau and the amyloid beta A4 protein,
  although generally fewer neurofibrillary tangles were positive for
  lactotransferrin than for tau protein. Neuronal cytoplasmic staining with
  lactotransferrin antibodies, was observed in a subpopulation of pyramidal
  neurons in normal aging, and was more pronounced in Alzheimer's disease,
  Guamanian cases, Pick's disease, and particularly in Down syndrome.
  Lactotransferrin was also strongly associated with Betz cells and other
  motoneurons in the primary motor cortex of control, Alzheimer's disease,
  Down syndrome, Guamanian and Pick's disease cases. These same
  lactotransferrin-immunoreactive motoneurons were severely affected in the
  cases with amyotrophic lateral sclerosis. It is possible that in these
  neurodegenerative disorders affected neurons either take up or synthesize
  lactotransferrin to an abnormally elevated rate. An excessive accumulation
  of lactotransferrin, as well as transported iron and aluminum, may lead to
  a cytotoxic effect resulting in the formation of intracellular lesions and
  neuronal death.
 
 
Authors
  Yasui M.  Ota K.  Garruto RM.
Institution
  Division of Neurological Diseases, Wakayama Medical College, Japan.
Title
  Concentrations of zinc and iron in the brains of Guamanian patients with
  amyotrophic lateral sclerosis and parkinsonism-dementia.
Source
  Neurotoxicology.  14(4):445-50, 1993 Winter.
Abstract
  Simultaneous measurements of zinc (Zn) and iron (Fe) concentrations were
  determined using neutron activation analysis in gray and white matter of
  the frontal and occipital regions obtained from four patients with
  parkinsonism-dementia (PD), eight with amyotrophic lateral sclerosis
  (ALS), and four neurologically normal controls from Guam. Zn content in
  gray matter from the frontal cortex in ALS and PD cases was significantly
  decreased, compared with that of controls (p < 0.05). No significant
  differences were found in the Zn content of white matter from the frontal
  cortex, and/or gray and white matter from the occipital cortex between the
  groups. The Zn content in gray matter from both frontal and occipital
  regions was less in ALS and PD patients than in controls. Fe content in
  gray matter from the frontal cortex of ALS and PD increased significantly
  compared with that of controls (p < 0.05). Fe content in white matter from
  the frontal cortex in PD patients was greater than in controls (p < 0.05),
  with an overall difference: controls < ALS < PD. These data indicate that
  an increase in Fe in gray and white matter, and a decrease concentration
  of Zn in gray matter, combined with an excess and deficiency of
  bioavailable aluminum and calcium, respectively, may be involved in the
  pathogenic process of these disorders.
 
 
Authors
  Semchuk KM.  Love EJ.  Lee RG.
Institution
  Department of Community Health Sciences, Faculty of Medicine, University
  of Calgary, Canada.
Title
  Parkinson's disease: a test of the multifactorial etiologic hypothesis.
Source
  Neurology.  43(6):1173-80, 1993 Jun.
Abstract
  We studied the relative etiologic importance upon the development of
  Parkinson's disease (PD) of occupational exposure to herbicides and other
  compounds, ionizing radiation exposure, family history of PD and essential
  tremor, smoking, and history of various viral and other medical
  conditions. We identified patients (n = 130) with neurologist-confirmed
  idiopathic PD through contacts with Calgary general hospitals, long-term
  care facilities, neurologists, the Movement Disorder Clinic, and the
  Parkinson's Society of Southern Alberta, and selected two matched (by sex
  and age +/- 2.5 years) community controls for each case by random digit
  dialing. We obtained lifetime work, chemical, radiation, medical, and
  smoking exposure histories and family histories of PD and essential tremor
  by personal interviews, and analyzed the data using conditional logistic
  regression for matched sets. After controlling for potential confounding
  and interaction between the exposure variables, using multivariate
  statistical methods, having a family history of PD was the strongest
  predictor of PD risk, followed by head trauma and then occupational
  herbicide use. Cases and controls did not differ in their previous
  exposures to smoking or ionizing radiation; family history of essential
  tremor; work-related contact with aluminum, carbon monoxide, cyanide,
  manganese, mercury, or mineral oils; or history of arteriosclerosis,
  chicken pox, encephalitis, hypertension, hypotension, measles, mumps,
  rubella, or Spanish flu. These results support the hypothesis of a
  multifactorial etiology for PD, probably involving genetic, environmental,
  trauma, and possibly other factors.
 
 
Authors
  Doering LC.
Institution
  Division of Anatomy, Faculty of Health Sciences, McMaster University,
  Hamilton, Ontario, Canada.
Title
  Probing modifications of the neuronal cytoskeleton. [Review]
Source
  Molecular Neurobiology.  7(3-4):265-91, 1993 Fall-Winter.
Abstract
  The prominent death of central neurons in Alzheimer's and Parkinson's is
  reflected by changes in cell shape and by the formation of characteristic
  cytoskeletal inclusions (neurofibrillary tangles, Lewy bodies). This
  review focuses on the biology of neurofilaments and microtubule-associated
  proteins and identifies changes that can occur to these elements from
  basic and clinical research perspectives. Attention is directed at certain
  advances in neurobiology that have been especially integral to the
  identification of epitope domains, protein isoforms, and posttranslational
  (phosphorylation) events related to the composition, development, and
  structure of the common cytoskeletal modifications. Recently, a number of
  experimental strategies have emerged to simulate the aberrant changes in
  neurodegenerative disorders and gain insight into possible molecular
  events that contribute to alterations of the cytoskeleton. Descriptions of
  specific systems used to induce modifications are presented. In
  particular, unique neural transplantation methods in animals have been
  used to probe possible molecular and cellular conditions concerned with
  abnormal cytoskeletal changes in neurons. [References: 255]
 
 
Authors
  Olanow CW.
Institution
  Department of Neurology, Psychiatry and Pharmacology, University of South
  Florida, Tampa.
Title
  A rationale for monoamine oxidase inhibition as neuroprotective therapy
  for Parkinson's disease. [Review]
Source
  Movement Disorders.  8 Suppl 1:S1-7, 1993.
Abstract
  Neurons in the substantia nigra may be vulnerable to oxidant stress
  because (a) the metabolism of dopamine generates peroxides, which, in the
  presence of iron, can lead to the formation of the highly reactive
  hydroxyl free radical; and (b) neuromelanin within nigral neurons can bind
  metals such as iron and aluminum and thereby promote the site-specific
  formation of free radicals. Postmortem studies show increased iron,
  decreased glutathione, and increased lipid peroxidation in the substantia
  nigra of patients with Parkinson's disease (PD). Recent studies also
  report iron and aluminum accumulation within neuromelanin granules of
  patients with PD. These findings suggest that the substantia nigra in the
  patient with PD is in a state of oxidant stress and that antioxidant
  therapy might protect residual dopamine neurons and slow the natural
  progression of PD. Selective inhibitors of monoamine oxidase type B
  (MAO-B) have been chosen for study because of their capacity to interfere
  with the oxidative metabolism of dopamine and so diminish the likelihood
  that free radicals will be formed. Initial studies demonstrate that the
  MAO-B inhibitor L-deprenyl (selegiline) delays the development of
  disability in otherwise untreated patients with early Parkinson's disease.
  Although the mechanism responsible for these observations remains unclear,
  these results are consistent with the possibility that L-deprenyl provides
  neuroprotective effects. [References: 46]
 
 
Authors
  Good PF.  Olanow CW.  Perl DP.
Institution
  Department of Pathology, Mt. Sinai Medical Center, New York, NY 10029.
Title
  Neuromelanin-containing neurons of the substantia nigra accumulate iron
  and aluminum in Parkinson's disease: a LAMMA study.
Source
  Brain Research.  593(2):343-6, 1992 Oct 16.
Abstract
  The Laser Microprobe Mass Analyzer (LAMMA) is a sensitive instrument for
  identifying and localizing trace elements in tissue samples. Using LAMMA,
  we have examined melanin-containing neurons of the substantia nigra in
  patients with Parkinson's disease (PD) and controls. We found that iron
  significantly accumulates within neuromelanin granules of patients with PD
  compared to controls. Increased aluminum was found in the neuromelanin
  granules of 2 of 3 PD cases but in no controls. The accumulation of iron
  and aluminum, which are known to promote oxidant stress, may account for
  the selective degeneration of neuromelanin-containing neurons in PD.
 
 
Authors
  Exley C.  Birchall JD.
Institution
  Institute of Aquaculture, University of Stirling, Scotland, U.K.
Title
  The cellular toxicity of aluminium.
Source
  Journal of Theoretical Biology.  159(1):83-98, 1992 Nov 7.
Abstract
  Aluminium is a serious environmental toxicant and is inimical to biota.
  Omnipresent, it is linked with a number of disorders in man including
  Alzheimer's disease, Parkinson's dementia and osteomalacia. Evidence
  supporting aluminium as an aetiological agent in such disorders is not
  conclusive and suffers principally from a lack of consensus with respect
  to aluminium's toxic mode of action. Obligatory to the elucidation of
  toxic mechanisms is an understanding of the biological availability of
  aluminium. This describes the fate of and response to aluminium in any
  biological system and is thus an important influence of the toxicity of
  aluminium. A general theme in much aluminium toxicity is an accelerated
  cell death. Herein mechanisms are described to account for cell death from
  both acute and chronic aluminium challenges. Aluminium associations with
  both extracellular surfaces and intracellular ligands are implicated. The
  cellular response to aluminium is found to be biphasic having both
  stimulatory and inhibitory components. In either case the disruption of
  second messenger systems is observed and GTPase cycles are potential
  target sites. Specific ligands for aluminium at these sites are unknown
  though are likely to be proteins upon which oxygen-based functional groups
  are orientated to give exceptionally strong binding with the free
  aluminium ion.
 
Authors
  Halliwell B.
Institution
  Division of Pulmonary-Critical Care Medicine, UC-Davis Medical Center,
  Sacramento 95817.
Title
  Reactive oxygen species and the central nervous system. [Review]
Source
  Journal of Neurochemistry.  59(5):1609-23, 1992 Nov.
Abstract
  Radicals are species containing one or more unpaired electrons, such as
  nitric oxide (NO.). The oxygen radical superoxide (O2.-) and the
  nonradical hydrogen peroxide (H2O2) are produced during normal metabolism
  and perform several useful functions. Excessive production of O2.- and
  H2O2 can result in tissue damage, which often involves generation of
  highly reactive hydroxyl radical (.OH) and other oxidants in the presence
  of "catalytic" iron or copper ions. An important form of antioxidant
  defense is the storage and transport of iron and copper ions in forms that
  will not catalyze formation of reactive radicals. Tissue injury, e.g., by
  ischemia or trauma, can cause increased metal ion availability and
  accelerate free radical reactions. This may be especially important in the
  brain because areas of this organ are rich in iron and CSF cannot bind
  released iron ions. Oxidative stress on nervous tissue can produce damage
  by several interacting mechanisms, including increases in intracellular
  free Ca2+ and, possibly, release of excitatory amino acids. Recent
  suggestions that free radical reactions are involved in the neurotoxicity
  of aluminum and in damage to the substantia nigra in patients with
  Parkinson's disease are reviewed. Finally, the nature of antioxidants is
  discussed, it being suggested that antioxidant enzymes and chelators of
  transition metal ions may be more generally useful protective agents than
  chain-breaking antioxidants. Careful precautions must be used in the
  design of antioxidants for therapeutic use. [References: 183]
 
 
Authors
  Yasui M.  Kihira T.  Ota K.
Institution
  Division of Neurological Diseases, Wakayama Medical College, Japan.
Title
  Calcium, magnesium and aluminum concentrations in Parkinson's disease.
Source
  Neurotoxicology.  13(3):593-600, 1992 Fall.
Abstract
  Concentrations of calcium (Ca) and aluminum (Al) were measured by neutron
  activation analysis and that of magnesium (Mg) by inductively coupled
  plasma emission spectrometry in 26 regions of Parkinson's disease (PD) and
  control brains. Ca concentration was unchanged in all anatomic subregions
  of PD brains compared with control brains. Mg concentration was lower in
  cortex, white matter, basal ganglia and brain stem of PD brains compared
  to control brains (p < 0.01). Al concentration in the substantia nigra,
  caudate nucleus and globus pallidus was higher in PD brains compared to
  controls (p < 0.05) and significantly higher in gray matter and the basal
  ganglia (p < 0.01). These studies are consistent with other observations
  linking high concentrations of Al and low levels of Mg in the pathogenesis
  of CNS degeneration and PD.
 
 
Authors
  Perl DP.  Good PF.
Institution
  Department of Pathology, Mount Sinai School of Medicine, New York, NY
  10029.
Title
  Aluminium and the neurofibrillary tangle: results of tissue microprobe
  studies. [Review]
Source
  Ciba Foundation Symposium.  169:217-27; discussion 227-36, 1992.
Abstract
  Despite the contradictory results of studies attempting to compare the
  bulk brain tissue aluminium content of specimens from Alzheimer's disease
  patients and controls, microprobe studies from our laboratory have
  consistently documented evidence of selective accumulation of the element
  within the neurofibrillary tangle-bearing cells associated with this
  condition. Laser microprobe mass analysis (a highly sensitive and precise
  technique for trace elemental microprobe analysis) has now demonstrated
  that the most prominent aluminium accumulations occur within the
  neurofibrillary tangle itself. Similar findings have been obtained from
  microprobe studies of the neurofibrillary tangles which are a
  characteristic feature of amyotrophic lateral
  sclerosis/parkinsonism-dementia complex of Guam. Although the
  intraneuronal localization of aluminium in the Guam-derived specimens is
  similar to that of Alzheimer's disease, the concentration of aluminium is
  considerably higher than is encountered in Alzheimer's disease specimens.
  We conclude that aluminium is an integral component of the neurofibrillary
  tangle and raise the possibility that the cross-linking properties of this
  highly reactive metal may stabilize the constituent cytoskeletal proteins
  which make up this pathological structure. [References: 37]
 
 
Authors
  Wisniewski HM.  Wen GY.
Institution
  New York State Institute for Basic Research in Developmental Disabilities,
  Staten Island 10314.
Title
  Aluminium and Alzheimer's disease. [Review]
Source
  Ciba Foundation Symposium.  169:142-54; discussion 154-64, 1992.
Abstract
  The hypothesis that aluminium (Al) is a cause of (or a risk factor in) the
  development of beta-amyloid plaques and neurofibrillary tangles (NFT) and
  dementia in Alzheimer's disease (AD) is based on studies by Wisniewski et
  al, Klatzo et al and Terry & Pena in 1965 that showed that injection of
  experimental animals with Al compounds induces the formation of NFT. Other
  publications revealed that Al affects cognitive functions in experimental
  animals and humans undergoing dialysis for renal failure. Electron probe
  and laser microprobe mass analysis (LAMMA) studies have demonstrated the
  presence of Al in NFT and cores of amyloid stars and nuclei of neurons in
  AD patients. Other studies have indicated the association between
  amyotrophic lateral sclerosis/Guam parkinsonism-dementia complex and Al in
  the environment. A recent report suggests that the chelating agent
  desferrioxamine slows the rate of cognitive decline in AD patients.
  Extensive studies of the pathology of AD and Al-induced encephalopathy by
  our group and others indicate that Al does not cause Alzheimer's disease
  neuropathology. However, under certain conditions, cognition can be
  affected when Al enters the brain. Therefore, for individuals with renal
  failure or undergoing dialysis or individuals with a damaged blood-brain
  barrier, the intake of Al should be controlled. [References: 46]
 
 
Authors
  Yasui M.  Kihira T.  Ota K.  Mukoyama M.  Adachi K.
Institution
  Division of Neurological Diseases, Wakayama Medical College.
Title
  [Aluminum deposition in the central nervous system tissues of patients
  with Parkinson's disease]. [Japanese]
Source
  Rinsho Shinkeigaku - Clinical Neurology.  31(10):1095-8, 1991 Oct.
Abstract
  Aluminum (Al) concentration in the 26 anatomic central nervous system
  (CNS) regions, liver, kidney, spleen and heart of our patients with
  Parkinson's disease, and five neurologically normal controls was measured
  by a non-destructive neutron activation analysis (NAA), in order to
  clarify the implication of Al on pathogenesis of Parkinson's disease. Al
  concentration in substantia nigra, caudate nucleus and globus pallidus
  increased in patients with Parkinson's disease more than that in controls
  (p less than 0.05). There was a significant difference in Al concentration
  of gray matter and basal ganglia in Parkinson's disease, compared with
  those of controls (p less than 0.01). It is likely that high Al deposition
  in pathological foci responsible for Parkinson's disease might be
  implicated in the pathogenesis of Parkinson's disease.
 
 
Authors
  Kiss SA.  Dombovari J.  Oncsik M.
Institution
  Borsod Chemical Works, Kazincbarcika, Hungary.
Title
  Magnesium inhibits the harmful effects on plants of some toxic elements.
Source
  Magnesium Research.  4(1):3-7, 1991 Mar.
Abstract
  Cadmium and aluminium ions - especially in acid soils - are taken up by
  plants which then become poisoned by them. As a result the roots of the
  plants become deformed, and the green parts become chlorotic and
  underdeveloped. The yield will thus be sharply reduced. Culture fluid and
  culture pot experiments have shown that the toxic effects can be inhibited
  by magnesium. Investigations have proved that the inhibition is
  competitive and is based on the antagonism of cadmium and aluminium
  towards magnesium. Toxic cadmium and aluminium concentrations in the soil
  can be decreased by the use of non-acidifying fertilizers, and inhibited
  or prevented with fertilizers containing magnesium, eg Agronit (28% N and
  2.5% Mg) or Kardonit (28% N and 5.5% Mg) (Borsod Chemical Works). Cadmium
  and aluminium taken up by plants are equally detrimental to animal and
  human organisms through the nutrition chain. For example cadmium may cause
  sterility, while aluminium may be implicated in Alzheimer's and
  Parkinson's disease. Magnesium moderates the effects of these two toxic
  elements in the human organism as well as in plants.
 
Authors
  Hirsch EC.  Brandel JP.  Galle P.  Javoy-Agid F.  Agid Y.
Institution
  INSERM U289, Hopital de la Salpetriere, Paris, France.
Title
  Iron and aluminum increase in the substantia nigra of patients with
  Parkinson's disease: an X-ray microanalysis.
Source
  Journal of Neurochemistry.  56(2):446-51, 1991 Feb.
Abstract
  The levels of different elements were studied by x-ray microanalysis in
  the substantia nigra and the central gray substance of patients with
  Parkinson's disease, progressive supranuclear palsy, and matched controls.
  In control brains, only iron, potassium, silicum, sodium, sulfur, and zinc
  were within the limit of detection of the technique. The abundance of each
  element was different, but their respective concentrations in the two
  brain regions were similar, except for sulfur levels which were higher on
  neuromelanin aggregates in the substantia nigra than in nigral regions
  lacking neuromelanin, and in the central gray substance. In Parkinson's
  disease, but not in progressive supranuclear palsy, nigral iron levels
  increased in regions devoid of neuromelanin and decreased on neuromelanin
  aggregates, but were unchanged in the central gray substance, when
  compared to control values. Concentrations of the other elements in the
  central gray substance and substantia nigra were not different from
  controls in brains from patients with Parkinson's disease and progressive
  supranuclear palsy. Analysis of Lewy bodies in the parkinsonian substantia
  nigra revealed high levels of iron and the presence of aluminum. Metal
  abundance was not affected in progressive supranuclear palsy, in spite of
  the nigral cell death. This suggests that the increased iron levels and
  the detection of aluminum observed in Parkinson's disease are not solely
  the consequence of the neuronal degeneration.
 
 
Authors
  Garruto RM.
Institution
  Laboratory of Central Nervous System Studies, National Institutes of
  Health, Bethesda, Maryland 20892.
Title
  Pacific paradigms of environmentally-induced neurological disorders:
  clinical, epidemiological and molecular perspectives. [Review]
Source
  Neurotoxicology.  12(3):347-77, 1991 Fall.
Abstract
  During the past quarter century biomedical scientists have begun to
  recognize the unique opportunities for studying disease etiology and
  mechanisms of pathogenesis in non-Western anthropological populations with
  focal, endemic diseases. Such natural experiments as they are called, are
  important paradigms for solving etiological and epidemiological problems
  of widespread medical significance, with an ultimate goal towards
  treatment and prevention. The systematic search for etiological factors
  and mechanisms of pathogenesis of neurodegenerative disorders is perhaps
  nowhere better exemplified than in the western Pacific. During the past
  three decades, the opportunistic and multidisciplinary study of
  hyperendemic foci of amyotrophic lateral sclerosis and
  parkinsonism-dementia which occur in different cultures, in different
  ecological zones and among genetically divergent populations have served
  as natural models that have had a major impact on our thinking and
  enhanced our understanding of these and other neurodegenerative disorders
  such as Alzheimer disease and the process of early neuronal aging. Our
  cross-disciplinary approach to these intriguing neurobiological problems
  and the accumulated epidemiological, genetic, cellular and molecular
  evidence strongly implicates environmental factors in their causation,
  specifically the role of aluminum and its interaction with calcium in
  neuronal degeneration. As a direct consequence of our studies in these
  Pacific populations, we have undertaken the long-term development of
  experimental models of neuronal degeneration, in an attempt to understand
  the cellular and molecular mechanisms by which these toxicants affect the
  central nervous system. Our experimental studies have resulted in the
  establishment of an aluminum-induced chronic myelopathy in rabbits and the
  development of neurofilamentous lesions after low-dose aluminum
  administration in cell culture. These studies clearly demonstrate the
  philosophy that chronic rather than acute experimental models of toxicity
  are necessary in order to enhance our understanding of human
  neurodegenerative disorders with long-latency and slow progression.
  Finally, the ultimate significance of these Pacific paradigms may well
  depend on our ability to comprehensively evaluate and synthesize the
  growing body of relevant scientific data from other human disorders and
  from widely divergent academic fields, as well as our ability to recognize
  emerging new models in nature. [References: 211]
 
Authors
  Wechsler LS.  Checkoway H.  Franklin GM.  Costa LG.
Institution
  Department of Environmental Health, University of Washington, Seattle
  98195.
Title
  A pilot study of occupational and environmental risk factors for
  Parkinson's disease.
Source
  Neurotoxicology.  12(3):387-92, 1991 Fall.
Abstract
  Increasingly, the etiology of Parkinson's disease (PD) has been linked to
  exposures to environmental toxicants. This epidemiologic pilot study used
  a self-administered questionnaire among 34 PD cases and 22 other neurology
  clinic control patients. All subjects were at least 40 years old. Risk
  factors investigated included occupation, well-water use, pesticide use,
  metal exposures, medical history, smoking, alcohol consumption, and drug
  use. Twenty-six percent of the male PD cases reported having been employed
  in farming versus eleven percent for male controls (OR = 3.1, 95% C.I. =
  0.3 to 35). Sixteen percent of male cases versus none of the controls
  reported employment as welders. No clear trends involving exposure to
  either occupational or home pesticides emerged. In assessing occupational
  exposures to metals, aluminum and copper exposures tended to be more
  common among male cases than male controls. Additionally, as reported in
  other studies, smoking showed an inverse relationship with PD. Although
  the findings reported here are provocative, these results are
  statistically imprecise and must be interpreted cautiously because of the
  small number of subjects included in the study.
 
 
Authors
  Perl DP.  Good PF.
Institution
  Department of Pathology, Arthur M. Fishberg Center for Neurobiology, Mount
  Sinai Medical Center, New York, New York 10029.
Title
  Aluminum, Alzheimer's disease, and the olfactory system. [Review]
Source
  Annals of the New York Academy of Sciences.  640:8-13, 1991.
Abstract
  In Alzheimer's disease, it has been recognized that there is a dramatic
  tendency for the development of neurofibrillary tangles among neurons of
  cortical regions associated with the olfactory system. We have
  demonstrated that neurofibrillary tangle-bearing neurons contain
  dramatically elevated levels of aluminum. The olfactory system, the only
  portion of the central nervous system with exposure to the external
  environment, is uniquely capable of uptake and transneuronal spread of
  exogenous substances. We argue that inasmuch as aluminum is not employed
  in any physiologic process, these deposits must arise from exogenous
  sources. Using parkinsonism-dementia complex of Guam as a model, we
  present data which suggest that the olfactory system is particularly
  vulnerable to damage and is affected very early in the disease. This
  supports the concept that etiologic agents of importance to this epidemic
  may be airborne in nature and may enter the central nervous system via the
  olfactory pathways. [References: 24]
 
Authors
  Youdim MB.  Ben-Shachar D.  Riederer P.
Institution
  Technion-Faculty of Medicine, Rappaport Family Research Institute, Haifa,
  Israel.
Title
  Iron in brain function and dysfunction with emphasis on Parkinson's
  disease. [Review]
Source
  European Neurology.  31 Suppl 1:34-40, 1991.
Abstract
  Metals such as lead, zinc, copper, aluminum and manganese have been
  implicated in neuropsychiatric disorders. However, until fairly recently
  the role of iron in brain function was rather obscure, because little
  attention was paid to its metabolism in the brain. It is now apparent that
  maintenance of brain iron homoeostasis is important for the normal
  functioning of his organ. Most of the studies have been directed towards
  the cognitive and attentional deficit resulting from nutritional iron
  deficiency. Evidence so far suggests subsensitivity of striatal dopamine
  neurotransmission. By contrast the selective increase in free iron in the
  substantia nigra pars compacta of parkinsonian brains is thought to
  initiate oxidative stress, from iron-induced liberation of cytotoxic
  oxygen free radicals. Such radicals are known to promote membrane
  fluidity, alteration in cellular calcium homoeostasis, lipid peroxidation
  and finally cell death in systemic organs. Evidence supporting similar
  processes being responsible for nigrostriatal dopamine neuron degeneration
  in Parkinson's disease is now becoming available. Such possibilities
  afford the development of neuroprotective drugs as a means to retard the
  progression of this disorder. These include other selective monoamine
  oxidase B inhibitors, iron chelators with the ability to cross the
  blood-brain barrier, selective calcium channel antagonists and
  mitochondrial electron transport system protectors. [References: 45]
 
 
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