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Review [Biochemical markers for Alzheimer disease] 2006
Czarna JM, Waldemar G, Heegaard NH. · Statens Serum Institut, Autoimmunafdelingen, og H:S Rigshospitalet, Hukommelsesklinikken, Neurologisk Afdeling. · Ugeskr Laeger. · Pubmed #16522291 No free full text.
Abstract: It is estimated that approximately 40,000 people in Denmark suffer from Alzheimer's disease (AD), a neurodegenerative dementia. Symptomatic treatment now exists which can temporarily inhibit the loss of brain function. Unfortunately, AD is difficult to diagnose, especially early in the disease course, and a definite diagnosis is possible only post-mortem. To develop improved diagnostic methods, several biomarkers have been examined for their ability to differentiate AD from normal aging and other dementias. Their measurement in blood samples has not yet been developed, but analyses may now be routinely performed using cerebrospinal fluid (CSF). The CSF biomarkers include amyloid-beta 1-42 (Abeta1-42), which is decreased in AD patients, as well as total tau (t-tau) and hyperphosphorylated tau (p-tau), which are elevated. While a decreased Abeta1-42 level in CSF has no independent value in the diagnostic differentiation, t-tau and p-tau add more specificity to the differentiation of AD from other dementias while retaining a reasonable degree of sensitivity.
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Article Years of severe and isolated amnesia can precede the development of dementia in early-onset Alzheimer's disease. 2005
Stokholm J, Jakobsen O, Czarna JM, Mortensen HV, Waldemar G. · Memory Disorders Research Unit, Neuroscience Centre, Copenhagen University Hospital, Rigshospitalet, Denmark. · Neurocase. · Pubmed #15804924 No free full text.
Abstract: A young patient with a severe and isolated memory disorder, meeting the criteria for MCI, was followed for a period of 8 years. His overall functional level remained stable with a CDR-score at 0.5 until the last year when it dropped to 1.0. Neuropsychological testing showed severe memory deficits but otherwise normal cognitive functions. Only minimal progression was measured; however, the last testing showed impaired abstraction and executive functioning as well as discrete problems generating names of objects and people. Neuroimaging, with MRI and SPECT, was consistent with a progressive degenerative disorder, and cerebrospinal fluid levels of beta-amyloid 1-42, tau protein, and phosphorylated tau protein were characteristic of Alzheimer's disease (AD). We argue that this is a case of prodromal AD, which illustrates an extreme version of the normal course with respect to slow progression of the disease and severity of amnesia early in the course.
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