Ischemia signalling to Alzheimer-related genes

Abstract

A b s t r a c t In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, preseni lins, apolipoproteins and secretases genes, playing key roles in β-amyloid peptide generation. Presented data are strongly supporting a hypothesis that brain ischemia may be involved in the aetiology of sporadic Alzheimer's disease. Potential contribution and impact of ischemically activated genes on the development of sporadic Alzheimer's disease remain to be established at both genetic and functional levels. The identification of the genes involved in sporadic Alzheimer

Review paper Neurogenesis and neuroprotection in postischemic brain neurodegeneration with Alzheimer phenotype: is there a role for curcumin?

“…Abnormal a-synuclein deposition might impair synaptic function, resulting in memory problems and additional postischemic neuronal death. Thus, the induction of amyloid precursor protein, apolipoproteins, presenilins and other Alzheimer's disease-related genes and proteins after ischemia may be the molecular link between Alzheimer's disease pathways and ischemia-reperfusion neurodegeneration [51,53]. As an effect of induction of the above genes there was noted long-term abnormal co-accumulation of amyloid precursor protein and amyloid precursor protein cleaving enzymes [52].…”

“…Dietary, genetic and molecular factors are important determinants in progression and treatment of the above diseases [1,[47][48][49][50][51]53]. In developed countries ischemic stroke is a major cause of physical disability, the third leading cause of mortality and the second most common cause of dementia [28,41].…”

Original article Mutations in the exon 7 of Trp53 gene and the level of p53 protein in double transgenic mouse model of Alzheimer’s disease

“…Alzheimer's disease (AD) is characterized both clinically by the decline of cognitive functions, such as memory, and pathologically by the presence of numerous senile plaques (SPs) and neurofibrillary tangles (NFTs) [2,3,28,40,46,51]. Neurofibrillary tangles consist of hyperphosphorylated tau protein, whereas Folia Neuropathologica 2014; 52/1 Trp53 and p53 in PS/APP mice SPs are composed of amyloid β-protein (Aβ).…”

Review article What causes alzheimer’s disease?

“…A further study of non-demented patients with critical coronary artery disease suggested that some patients had similar densities of SP to AD, numbers of SP being directly proportional to the duration of arterial disease [181]. In addition, there may a close link between ischaemic brain episodes and sporadic cases of AD (SAD) suggesting that neovascular factors could aggravate the progression of the disease [150,151].…”