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Article Abnormal short latency afferent inhibition in early Alzheimer's disease: a transcranial magnetic demonstration. 2008
Nardone R, Bergmann J, Kronbichler M, Kunz A, Klein S, Caleri F, Tezzon F, Ladurner G, Golaszewski S. · Department of Neurology, Christian Doppler Clinic, Paracelsus Private Medical University Salzburg, Salzburg, Austria. · J Neural Transm. · Pubmed #18841323 No free full text.
Abstract: The pathogenesis of Alzheimer's disease (AD) appears to involve several different mechanisms, the most consistent of which is an impairment of cholinergic neurotransmission; however, there is controversy about its relevance at the early stage of disease. A transcranial magnetic stimulation (TMS) protocol based on coupling peripheral nerve stimulation with motor cortex TMS (short latency afferent inhibition, SAI) may give direct information about the function of some cholinergic pathways in the human motor cortex. We evaluated SAI in a group of patients with early diagnosis of AD and compared the data with that from a control group. The amount of SAI was significantly smaller in early AD patients than in controls. This study first provides physiological evidence that a central cholinergic dysfunction occurs in the earlier stages of AD. Identification of SAI abnormalities that occur early in the course of AD will allow earlier diagnosis and treatment with cholinergic drugs.
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Article A broader horizon of Alzheimer pathogenesis: ALZAS--an early serum biomarker? 2002
Kienzl E, Jellinger K, Janetzky B, Steindl H, Bergmann J. · Vienna Health Board and L. B. Institute of Clinical Neurobiology, Vienna, Austria. · J Neural Transm Suppl. · Pubmed #12456054 No free full text.
Abstract: Recently, a novel risk gene protein expressed in elderly patients with the diagnosis of Alzheimer disease (AD) was discovered on chromosome 21 within the APP (amyloid precursor protein) region. This 79 amino acid protein, ALZAS (Alzheimer Associated Protein) contains the beta-amyloid peptide 1-42 fragment, the APP transmembrane signal, and a unique 12 amino acid c-terminal which is not present in any known allele of the APP gene. Reverse transcription-PCR revealed that the transcript of ALZAS was expressed in cortical and hippocampal regions of human Alzheimer disease brain as well as in leukocytes derived from AD patients. Most specifically, an endogenous antibody was found in patients with confirmed AD, in patients with depression, and in subjects suggested to have presymptomatic AD, where it was directed against epitopes within the intron encoded amino acid c-terminal sequence.
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Minor Alternatives to the suspended Alzheimer's disease vaccine. 2002
Bergmann J, Kienzl E, Janetzky B, Preddie E, Jellinger KA. · No affiliation provided · Acta Neuropathol. · Pubmed #12070673 No free full text.
This publication has no abstract.
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