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Therapeutic strategies for Alzheimer's disease based on new molecular mechanisms

100%
Religa D., Winblad B.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 4
393-396
EN
Background and objective: Alzheimer's disease (AD) ? the main cause of dementia ? is characterized by the presence of neuritic plaques containing the amyloid-beta peptide (A beta) and an intraneuronal accumulation of tubule-associated protein called tau. The current and future therapeutic strategies for AD will be discussed. Currently available treatment used in AD is based on acetylcholinesterase inhibitors, since in the course of AD there is a substantial loss in cholinergic neurons. Another registered drug used in more severe AD is NMDA antagonist ? memantine. Available strategies for AD include vitamin supplementation for reducing homocysteine levels, statins and non-steroidal anti-inflammatory drugs. The big hope of the last few years ? vitamin E and estrogen supplementation have not been proved efficient, but more studies are needed. There are several strategies aimed at acting directly on A beta or amyloid precursor protein (APP) processing: vaccination with A beta peptide, A beta passive immunization, beta and gamma secretases inhibitors. Nerve growth factors and neurotrophines could also be targeted by new therapies. Conclusions: a better understanding of the role of APP processing and folate and homocysteine in neuronal homeostasis throughout life consist revealing novel and relatively inexpensive approaches for preventing and treating AD.
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Thyroid function in patients with Alzheimer's disease treated with cholinesterase inhibitors

80%
Kapaki E., Ilias I., Paraskevas G. P., Theotoka I., Christakopoulou I.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 4
389-392
EN
The aim of the present study was to explore a possible interplay between cholinesterase inhibitors (ChEIs) and thyroid function tests (TFTs) in patients with Alzheimer's disease (AD). We reviewed thyroid function tests in 19 patients with AD before and after treatment (Rx) with ChEIs. Immunoradiometric assays were used for measuring serum thyrotropin, free thyroxin (FT4) and free triiodothyronine (FT3). Significant differences were observed among FT3 levels according to the duration of therapy. Subtle variations in thyroid function tests - before and after therapy - could be possibly related to ChEIs-induced altered thyroid function.
3
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Serotoninergic impairment and aggressive behavior in Alzheimer's disease

80%
Zarros A. C., Kalopita K. S., Tsakiris S. T.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 3
277-286
EN
The overall goal of all therapeutic interventions in Alzheimer's disease (AD) is to: (a) optimize the impaired functions and (b) restore an affordable quality of life for both the patient and his surroundings. AD has been characterized by a significant serotoninergic impairment. It is well known that impaired serotoninergic function is related to aggressive behavior. We, herein, review the past and recent evidence that seems to link the serotoninergic system with aggressive manifestations in AD patients. Managing the aggressive behavior of these patients might be of significant medical, social and economical importance. However, there is still a long way to go until we verify the exact pathophysiological mechanism(s) involved in the induction of aggression in AD patients. The current data underlines a complex relationship between the observed serotoninergic impairment in AD patients and the (a) cholinergic system, (b) the endocrine (hormonal) state, (c) the nutritional habits, (d) the genetic background and (e) the caregiving environment.
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Plasma levels of alphabeta peptides are altered in amnestic mild cognitive impairment but not in sporadic Alzheimer's disease

80%
Sobow T., Flirski M., Kloszewska I., Liberski P. P.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
117-124
EN
Plasma AlphaBeta levels have been examined in sporadic Alzheimer's disease yielding conflicting results; both no difference and an increase in plasma concentrations of A1-42 and A1-40 in sporadic cases of AD as compared to controls have been reported. Elevated plasma A1-42 levels may be detected several years before the onset of symptoms (in mild cognitive impairment stadium). Levels of AlphaBeta140 and AlphaBeta142 were measured in plasma from 54 patients with AD, 39 subjects with MCI and 35 controls using a commercially available ELISA. Mean plasma AlphaBeta142 levels were significantly higher in MCI as compared to both AD (P<0.001) and control subjects (P<0.001), while AlphaBeta140 did not differ between the groups. No correlations were observed between A levels and age, MMSE scores or gender. According to ROC curve analysis the maximum accuracy in discriminating MCI versus both controls and AD subjects has been achieved using a cut-off value of 3.8.
5
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Plasma Abeta levels as predictors of response to rivastigmine treatment in Alzheimer's disease

80%
Sobow T., Flirski M., Liberski P., Kloszewska I.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 2
131-139
EN
Cholinesterase inhibitors are currently the mainstream of symptomatic treatment of patients with Alzheimer's disease. The response to treatment with cholinesterase inhibitors is clinically difficult to predict. Several demographic, clinical and biological variables have been proposed as pretreatment predictors of long-term therapy efficacy. In this paper, consistently with previous reports, we confirm that higher initial disease severity and faster progression of cognitive impairment increase the chance of a clinically meaningful response to cholinesterase inhibitor therapy in a carefully selected population of patients with Alzheimer's disease. Moreover, for the first time we demonstrate the association between the increase in the concentration of plasma Abeta(1-42) peptide after 2 weeks of treatment with an initial dose of rivastigmine and the likelihood of a positive response to treatment after 6 months. A change in plasma Abeta(1-42) level might constitute a novel biochemical predictor of rivastigmine treatment efficacy in Alzheimer's disease.
6

The influence of aging in one tauopathy: Alzheimer 's disease

80%
Avila J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
410-413
EN
In this short review, the link between aging and the onset of Alzheimer's disease is discussed. It has been widely suggested that aging is the greatest risk factor for Alzheimer's disease, in which a failure in the insulin signal-transduction pathway could occur with age and, thereby, the assembly of senile plaques and neurofibrillary tangles (two aberrant structures present in Alzheimer's disease) could be promoted. The main component of neurofibrillary tangles is the microtubule-associated protein tau, and the assembly of tau protein appears to occur after its modification by phosphorylation. In this phosphorylation, some protein kinases related to the insulin-transduction pathway could play a role.
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Oxidative DNA damage and level of thiols as related to polymorphisms of MTHFR, MTR, MTHFD1 in Alzheimer's and Parkinson's diseases

70%
Dorszewska J., Florczak J., Rozycka A., Kempisty B., Jaroszewska-Kolecka J., Chojnacka K., Trzeciak W. H., Kozubski W.
Acta Neurobiologiae Experimentalis
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2007
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vol. 67
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issue 2
113-129
EN
Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are accompanied by increased levels of 8-oxo-2'-deoxyguanosine (8-oxo2dG) and alterations in levels of homocysteine (Hcy), methionine (Met), and cysteine (Cys). Hcy may undergo remethylation due to involvement of MTHFR, MTR and MTHFD1 proteins. Present studies are aimed at determination of 8-oxo2dG, Hcy, Met, and Cys in AD and PD patients as well as in control groups, using HPLC/EC/UV, as well as estimation, by restriction analysis, frequency of following gene polymorphisms: MTHFR (C677T, A1298C, G1793A), MTHFD1 (G1958A), and MTR (A2756G). In AD there were significant differences of the levels of only Cys (GG, MTHFR, G1793A) and Met/Hcy (AA, MTHFD1, G1958A) whereas in PD there were more significant differences of the levels of thiols: Hcy [MTHFR: CT (C677T) and GG (G1793A); MTR, AG (A2756G)], Met [MTR, AA (A2756G)], Cys [MTR, AG (A2756G)], and Met/Hcy [MTHFR: CC, CT (C677T) and AA (A1298C), and GG (G1793A); MTHFD1 AA(G1958A); MTR AA(A2756G)]. Significant differences in the levels of Cys/Hcy, MTHFD1 GA (G1958) were varied between AD and PD groups. The results indicate that of the enzymes studied only polymorphisms of folate-dependent enzyme MTHFD1 have pointed to significant differences in intensity of turnover of circulating thiols between AD and PD patients.
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Dysregulation of calcium in Alzheimer's disease

70%
Brzyska M., Danek E.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 3
171-183
EN
Multiple efforts has underlined importance of calcium dependent cellular processes in the biochemical characterisation of Alzheimer?s disease (AD), suggesting that abnormalities in calcium (Ca2+) homeostasis might be involved in the pathophysiology of the disease. Studies of the pathogenic mutations in presenilins 1 and 2 (PS1 and PS2) and amyloid precursor protein (APP) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis. Studies of apolipoprotein E (ApoE) neurotoxic effects in AD confirmed involvement of Ca2+-mediated mechanisms. Futher consequences of Ca2+ alterations in AD underline the importance of the ER and mitochondria as the regulatory sites involved in the pathogenesis of neuronal degeneration. Alterations of Ca2+ homeostasis include cells from peripheral tissues, including lymphocytes and fibroblasts from AD donors.
9
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Mitochondrial DNA in pathogenesis of Alzheimer's and Parkinson's diseases

61%
Maruszak A., Gaweda-Walerych K., Soltyszewski I., Zekanowski C.
Acta Neurobiologiae Experimentalis
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2006
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vol. 66
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issue 2
153-176
EN
A critical role of mitochondrial dysfunction and oxidative damage has been implicated in etiopathology of many neurodegenerative disorders, as well as in normal aging. Alzheimer's and Parkinson's diseases are common devastating late-onset neurodegenerative disorders, associated with mitochondrial DNA variations, which are suggested to affect mitochondrial functions. This paper reviews the current knowledge on the inherited and somatic mtDNA variations in both conditions.
10
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Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

51%
Zekanowski C., Wojda U.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 2
232-253
EN
Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.
11
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Alzheimer's beta-amyloid peptide as a source of neurotoxic free radicals: the role of structural effects

41%
Pogocki D.
Acta Neurobiologiae Experimentalis
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2003
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vol. 63
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issue 2
131-145
EN
This mini review gives a brief overview over the oxidation mechanism of methionine (Met), relevant for processes which may lead to the oxidation of amyloid beta-peptide (betaAP), involved in the pathogenesis of Alzheimer?s disease. The Cu II-catalysed oxidation of C-terminal Met 35 in AP depends on the secondary structure of the peptide. That seems to be the key to the known propensities of this peptide to form reactive oxygen species and free radicals. The pro-oxidant character of betaAP is not associated with its -beta sheet insoluble form. On the contrary, the alpha-helically organised structure is responsible for betaAP redox-related cytotoxicity.
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