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Dysregulation of calcium in Alzheimer's disease

100%

Brzyska M., Danek E.

Acta Neurobiologiae Experimentalis

2003

vol. 63

issue 3

171-183

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.

Neurodegenerative aspects of protein aggregation

81%

Trzesniewska K., Brzyska M., Elbaum D.

Acta Neurobiologiae Experimentalis

2004

vol. 64

issue 1

41-52

Protein aggregation and amyloid fibril deposits are characteristic features of more than twenty pathologic conditions characterized by plaque deposition in the central nervous system. Recent studies point out relationships between protein misfolding and numerous serious diseases. Despite different origins (sporadic, familial or transmissible), they are sometimes called conformational diseases to emphasize aberrant conformations as the putative cause of deposits that precede or accompany the clinical manifestation of the disease. Neurological disorders such as Alzheimer's disease (AD), Prion disorders (PrD), Parkinson's disease (PD), and Huntington's disease (HD) are the most typical examples of protein-based dementias, characterized by protein conformational transitions (alpha-helix/random coil to beta-sheet) that cause aggregation followed by fibrillization. Although it is very tempting to postulate a common mechanism of toxicity based on conformational and structural analogies, it should be noted that the factors responsible for conformational transition, oligomerization, aggregation, and plaque formation, are still subject of speculation and additional data is required to test the amyloid fibril hypothesis.

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2 Acta Neurobiologiae Experimentalis

1 2004

1 2003

2 Brzyska M.

1 Danek E.

1 Elbaum D.

1 Trzesniewska K.

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Dysregulation of calcium in Alzheimer's disease

Neurodegenerative aspects of protein aggregation