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Aluminum (Al)

Source. Aluminum (Al) is ubiquitous in its oxidized form, present in air, food, and water. Its main industrial use is in the metal working industries. Aluminum hydroxide is frequently used as an antacid without producing clinical symptoms. However,

Reusche/Luebeck

Nebenniere

25/92-3

SPEKTRUM 1830 POLARITY + RANGE ,25 V

3/2/1993 LASER uJ [131101 8]

Reusche/Luebeck

Nebenniere

25/92-3

SPEKTRUM 1830 POLARITY + RANGE ,25 V

3/2/1993 LASER uJ [131101 8]

Ag iilii

Fig. 17.1a-d. Dialysis-associated encephalopathy. a Hypoglossal neuron with pathognomonic deeply black, fine-granular cytoplasmic inclusions in dialysis-associated encephalopathy in comparison with the brownish neuronal lipofuscin in neurons of the inferior olivary nucleus (b - silver staining; X2000). c Laser microprobe mass analysis with aluminum peak at m/z 27, confirming the high aluminum content of silver-stained inclusions (peaks at m/z 104 and 106 result from silver staining). d Electron microscopy with partly electron-dense, partly bizarre electron-lucent material of (aluminum-containing) inclusions (X40,000). The figure was kindly provided by Professor Dr. E. Reusche, Lübeck

Fig. 17.1a-d. Dialysis-associated encephalopathy. a Hypoglossal neuron with pathognomonic deeply black, fine-granular cytoplasmic inclusions in dialysis-associated encephalopathy in comparison with the brownish neuronal lipofuscin in neurons of the inferior olivary nucleus (b - silver staining; X2000). c Laser microprobe mass analysis with aluminum peak at m/z 27, confirming the high aluminum content of silver-stained inclusions (peaks at m/z 104 and 106 result from silver staining). d Electron microscopy with partly electron-dense, partly bizarre electron-lucent material of (aluminum-containing) inclusions (X40,000). The figure was kindly provided by Professor Dr. E. Reusche, Lübeck clinical features attributed to aluminum intoxication have been described after chronic dialysis (see also p. 613 f) with dialysis fluid containing aluminum as well as following oral administration of phosphate-binding agents containing aluminum (McLaughlin et al. 1962; Alfrey et al. 1976; Elliott et al. 1978; Mar-tyn et al. 1989). A relationship has been hypothesized between exposure to aluminum in food and water and Alzheimer's disease (Wisniewski et al. 1979). The normal concentration of aluminum in the brain is <10 (ag/l, which increases with age.

Pathogenesis. If the blood contains elevated levels of aluminum in association with a compromised blood-brain barrier (McDermott et al. 1978), the brain will also have elevated levels of aluminum (Crapper McLachlan et al. 1983). Plasma levels above 100 (g/l are potentially toxic; levels exceeding 500 (g/l are indicative of acute aluminum poisoning. At the cellular level, aluminum is known to disrupt the slow transport of neurofilament proteins (NFP), which leads to an accumulation of NFP at the proximal end of the axon (Bizzi et al. 1984; Bin and Gar-finkel 1994) and a proliferation of microfilaments in the perikaryon (Klatzo et al. 1965; Weinstein 1974).

The similarity of clinical symptoms in association with elevated levels of aluminum demonstrated in the brains of victims of dementia of Alzheimer type (Crapper McLachlan et al. 1983) has given rise to a theory that Alzheimer's disease may be caused by an accumulation of aluminum in the brain (Martyn et al. 1989). This hypothesis has fallen out of favor.

Clinical Features. Aluminum poisoning is characterized by progressive dementia with speech impairment, myoclonus, focal and/or generalized epileptic seizures, focal neurological symptoms, and loss of consciousness. An aluminum-induced degeneration of motor neurons must be distinguished from a dialysis encephalopathy. The disease can end in death. The differential diagnosis must include Alzheimer's disease. Desferrioxamine is the specific chelating antidote.

Morphology. The morphological changes caused by aluminum intoxication are non-characteristic in H&E preparations (McLaughlin et al. 1962). Ganglion cells are shrunken, but usually there is no clear decline in their numbers. Some differences can be demonstrated immunohistochemically: in aluminum poisoning, neurons do not react to microtubule-as-sociated protein 2 (MAP-2), p-tubulin or ubiquitin, while in Alzheimer's disease they do (Strong et al. 1991). Aluminum poisoning is also associated with proliferation of microglia and astrocytes as well as a spongiform disintegration of the neuropil in the second and third cortical layer.

Using new variants of silver staining, Reusche described in 1991 a new effective method for the demonstration of Alzheimer changes by light- and electron microscopy (Reusche et al. 1992). The same methods allowed for the first time the demonstration in ten long-term hemodialyzed patients of characteristic and pathognomonic aluminum-containing inclusions in the cytoplasm of choroid plexus epithelia, glia, and neurons of the CNS (Reusche and Seydel 1993). Argyrophilic proteinaceous deposits of this "dialysis-associated encephalopathy" (DAE) were shown by light- and electron microscopy. They obviously result from long-standing and futile cyto-plasmic lysosomal degradation of aluminum. Similar deposits could be demonstrated in peripheral organs as well (Reusche et al. 1996). Laser microprobe mass analysis confirmed high cellular levels of aluminum (Fig. 17.1). The morphology is completely different from neuronal changes in Alzheimer's disease (Reusche and Seydel 1993; Reusche 1997). The evaluation of 50 long-term hemodialyzed patients -with ingestion of aluminum-containing drugs, up to 2.5 kg "pure" aluminum - presented no increase in the incidence of Alzheimer's disease (Reusche et al. 2001).

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