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  • 1
    Electronic Resource
    Electronic Resource
    Alzheimer's peptide kills cells of retina in vivo (1998)
    [s.l.] : Macmillan Magazines Ltd.
    Nature 392 (1998), S. 140-141 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Alzheimer's disease, the commonest form of dementia, is a progressive, age-dependent disorder characterized by the presence of large numbers of senile plaques and neurofibrillary tangles. The neuritic plaques consist of an accumulation of amyloid-β peptide (Aβ); this substance, which ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/32327
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  • 2
    Electronic Resource
    Electronic Resource
    Markers of axonal injury in post mortem human brain (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 433-439 
    Details
    ISSN: 1432-0533
    Keywords: Key words Immunocytochemistry ; β-Amyloid precursor protein ; Diagnostic tests ; routine ; Diffuse axonal injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-Amyloid precursor protein (βAPP) can be detected immunocytochemically at sites of axonal injury in the brain, and has recently been found to be a useful marker for injured axons in patients who survived for only 3   h after head trauma. It is transported by fast axonal transport and is thought to accumulate in detectable levels where the cytoskeleton breaks down. If this theory is correct, other substances should accumulate here in the same way, so we have used antibodies to other neuronal proteins to compare their efficacy as markers of axonal injury. SNAP-25, chromogranin A and cathepsin D also marked injured axons at all survival times studied (2.5   h – 2 weeks), although they were not as sensitive or specific as βAPP. Immunolabelling for the 68-kDa neurofilament subunit (NF68) was present in most uninjured axons, and allowed axonal swellings to be seen in some cases. Synaptophysin, GAP-43, ubiquitin or tau did not label any normal or injured axons in this study. We, therefore, suggest that βAPP should be the immunocytochemical marker of choice for the detection of injured axons. This study also showed that microwave antigen retrieval significantly enhances the immunoreactivity of SNAP-25, chromogranin A, synaptophysin, GAP-43, ubiquitin and tau, in addition to that of βAPP, in formalin-fixed, paraffin-embedded tissue, and reveals NF68 antigenicity where it was not previously detectable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00389495
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  • 3
    Electronic Resource
    Electronic Resource
    Markers of axonal injury in post mortem human brain (1994)
    Springer
    Acta neuropathologica 88 (1994), S. 433-439 
    Details
    ISSN: 1432-0533
    Keywords: Immunocytochemistry ; β-Amyloid precursor protein ; Diagnostic tests, routine ; Diffuse axonal injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-Amyloid precursor protein (βAPP) can be detected immunocytochemically at sites of axonal injury in the brain, and has recently been found to be a useful marker for injured axons in patients who survived for only 3 h after head trauma. It is transported by last axonal transport and is thought to accumulate in detectable levels where the cytoskeleton breaks down. If this theory is correct, other substances should accumulate here in the same way, so we have used antibodies to other neuronal proteins to compare their efficacy as markers of axonal injury. SNAP-25, chromogranin A and cathepsin D also marked injured axons at all survival times studied (2.5h–2 weeks), although they were not as sensitive or specific as βAPP. Immunolabelling for the 68-kDa neurofilament subunit (NF68) was present in most uninjured axons, and allowed axonal swellings to be seen in some cases. Synaptophysin, GAP-43, ubiquitin or tau did not label any normal or injured axons in this study. We, therefore, suggest that βAPP should be the immunocytochemical marker of choice for the detection of injured axons. This study also showed that microwave antigen retrieval significantly enhances the immunoreactivity of SNAP-25, chromogranin A, synaptophysin, GAP-43, ubiquitin and tau, in addition to that of βAPP, in formalin-fixed, paraffin-embedded tissue, and reveals NF68 antigenicity where it was not previously detectable.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00389495
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Axonal injury: a universal consequence of fatal closed head injury? (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 537-543 
    Details
    ISSN: 1432-0533
    Keywords: β-Amyloid precursor protein ; Head injury ; Diffuse axonal injury ; Immunocytochemistry ; Diagnosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-Amyloid precursor protein immunostaining has recently been shown to be a reliable method for detecting the damage to axons associated with fatal head injury. In an attempt to compare the efficacy of this technique with conventional histological detection of axonal damage, we have reanalysed sections from a large well-characterised series of head-injured and control patients. The results indicate that the frequency of axonal injury has been vastly underestimated using conventional silver techniques, and that axonal injury may in fact be an almost universal consequence of fatal head injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571509
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  • 5
    Electronic Resource
    Electronic Resource
    Axonal injury: a universal consequence of fatal closed head injury? (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 537-543 
    Details
    ISSN: 1432-0533
    Keywords: Key words β-Amyloid precursor protein ; Head injury ; Diffuse axonal injury ; Immunocytochemistry ; Diagnosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-Amyloid precursor protein immunostaining has recently been shown to be a reliable method for detecting the damage to axons associated with fatal head injury. In an attempt to compare the efficacy of this technique with conventional histological detection of axonal damage, we have reanalysed sections from a large well-characterised series of head-injured and control patients. The results indicate that the frequency of axonal injury has been vastly underestimated using conventional silver techniques, and that axonal injury may in fact be an almost universal consequence of fatal head injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571509
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Is β-APP a marker of axonal damage in short-surviving head injury? (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 608-613 
    Details
    ISSN: 1432-0533
    Keywords: Key words Head injury ; Axonal bulbs ; β-amyloid ; precursor protein (β-APP) ; Immunocytochemistry ; Diffuse axonal injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract β-Amyloid precursor protein (β-APP), a normal constituent of neurons which is conveyed by fast axonal transport, has been found to be a useful marker for axonal damage in cases of fatal head injury. Immunocytochemistry for β-APP is a more sensitive technique for identifying axonal injury than conventional silver impregnation. This study was designed to determine how quickly evidenc of axonal damage and bulb formation appears. Using this method a variety of brain areas were studied from 55 patients who died within 24 h of a head injury. Immunocytochemical evidence of axonal injury was first detected after 2 h survival, axonal bulbs were first identified after 3 h survival, and the amount of axonal damage and axonal bulb formation increased the longer the survival time.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050568
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  • 7
    Electronic Resource
    Electronic Resource
    A demonstration of the advantages of immunostaining in the quantification of amyloid plaque deposits (1989)
    Springer
    Histochemistry and cell biology 92 (1989), S. 355-358 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Extracellular amyloid deposits are a feature of both Alzheimer type dementia and the ‘normal’ aging process. Quantification of amyloid plaque deposits may well be useful in distinguishing between the senescent changes associated with ‘normal’ aging and the pathological processes underlying dementia. To determine the most reliable and reproducible method for visualisation of the amyloid we have compared conventional silver staining techniques with β-amyloid immunocytochemistry on a large sample of post-mortem brain tissue from both demented (n=15, age range 60–87) and non-demented (n=65, age range 14–99) patients. The degree of amyloid deposition was rated on a four point scale and ratings for the two techniques were significantly correlated (P〈0.01). However, the immunocytochemical approach has a number of distinct advantages for quantification. The antibody to β-amyloid is highly specific and does not stain neurofibrillary tangles or background features, it is considerably more sensitive than silver staining in highlighting diffuse amyloid deposits and, perhaps most importantly, it produces high contrast staining which allows easier image digitisation and subsequent computer image analysis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500553
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  • 8
    Electronic Resource
    Electronic Resource
    Is There a Genetic Basis for the Deposition of β-Amyloid After Fatal Head Injury? (1999)
    Springer
    Cellular and molecular neurobiology 19 (1999), S. 19-30 
    Details
    ISSN: 1573-6830
    Keywords: head injury ; β-APP metabolism ; β-amyloid ; apolipoprotein E
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. Alzheimer's disease is a heterogeneous disorder that may be caused by genetic or environmental factors or by a combination of both. Abnormalities in chromosomes 1, 14, and 21 have all been implicated in the pathogenesis of the early-onset form of the disease, while the ε4 allele of the apolipoprotein E gene (on chromosome 19) is now recognized as a risk factor for early- and late-onset sporadic and familial Alzheimer's disease. 2. The best-established environmental trigger for the disease is a head injury, based on epidemiological and neuropathological evidence. Approximately 30% of patients who die after a single episode of severe head injury show intracerebral deposition of β-amyloid protein (Aβ), a protein that is thought to be central to the pathogenesis of Alzheimer's disease. 3. Recent studies have revealed an over-representation of the apoE ε4 allele in those head-injured patients displaying Aβ pathology, thus providing the first evidence for a link between a genetic susceptibility (apoE ε4) and an environmental trigger (head injury) in the development of Alzheimer-type pathology.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006956306099
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