“…New risk factors have also been identified including those associated with diet such as obesity [31,71,125,185], diabetes [4,118,124] and factors associated with the immune system [12,128,141,158]. With reference to metal exposure, the case for aluminium is less strong but other metals such as zinc and copper have been implicated, and the interactions among different metals emphasised [16,86,147,156]. Recent data have also increased the probability that exposure to infectious agents could be involved [89].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, a significant proportion of the population are routinely exposed to trace metals such as aluminium, lead, iron, and copper, obtained from a variety of sources, and all are potential risk factors for AD [86]. Arsene et al [16], however, reported no relationship between metal accumulation with age or neurodegeneration suggesting the brain was not a favourable site for metal accumulation.…”
Early reviews identified over 20 risk factors associated with Alzheimer's disease (AD) including age, familial inheritance, exposure to aluminium, traumatic brain injury (TBI), and associated co-morbidities such as vascular disease and infection. In the light of recent evidence, this review reconsiders these risk factors, identifies those currently regarded as important, and discusses various hypotheses to explain how they may cause AD. Rare forms of early-onset familial AD (EO-FAD) are strongly linked to causal gene mutations, viz. mutations in amyloid precursor protein (APP) and presenilin (PSEN1/2) genes. By contrast, late-onset sporadic AD (LO-SAD) is a multifactorial disorder in which age-related changes, genetic risk factors, such as allelic variation in apolipoprotein E (Apo E) and many other genes, vascular disease, TBI and risk factors associated with diet, the immune system, mitochondrial function, metal exposure, and infection are all implicated. These risk factors may act collectively to cause AD pathology: 1) by promoting the liberation of oxygen free radicals with age, 2) via environmental stress acting on regulatory genes early and later in life ('dual hit' hypothesis), or 3) by increasing the cumulative 'allostatic load' on the body over a lifetime. As a consequence, lifestyle changes which reduce the impact of these factors may be necessary to lower the risk of AD.
“…New risk factors have also been identified including those associated with diet such as obesity [31,71,125,185], diabetes [4,118,124] and factors associated with the immune system [12,128,141,158]. With reference to metal exposure, the case for aluminium is less strong but other metals such as zinc and copper have been implicated, and the interactions among different metals emphasised [16,86,147,156]. Recent data have also increased the probability that exposure to infectious agents could be involved [89].…”
Section: Discussionmentioning
confidence: 99%
“…In addition, a significant proportion of the population are routinely exposed to trace metals such as aluminium, lead, iron, and copper, obtained from a variety of sources, and all are potential risk factors for AD [86]. Arsene et al [16], however, reported no relationship between metal accumulation with age or neurodegeneration suggesting the brain was not a favourable site for metal accumulation.…”
Early reviews identified over 20 risk factors associated with Alzheimer's disease (AD) including age, familial inheritance, exposure to aluminium, traumatic brain injury (TBI), and associated co-morbidities such as vascular disease and infection. In the light of recent evidence, this review reconsiders these risk factors, identifies those currently regarded as important, and discusses various hypotheses to explain how they may cause AD. Rare forms of early-onset familial AD (EO-FAD) are strongly linked to causal gene mutations, viz. mutations in amyloid precursor protein (APP) and presenilin (PSEN1/2) genes. By contrast, late-onset sporadic AD (LO-SAD) is a multifactorial disorder in which age-related changes, genetic risk factors, such as allelic variation in apolipoprotein E (Apo E) and many other genes, vascular disease, TBI and risk factors associated with diet, the immune system, mitochondrial function, metal exposure, and infection are all implicated. These risk factors may act collectively to cause AD pathology: 1) by promoting the liberation of oxygen free radicals with age, 2) via environmental stress acting on regulatory genes early and later in life ('dual hit' hypothesis), or 3) by increasing the cumulative 'allostatic load' on the body over a lifetime. As a consequence, lifestyle changes which reduce the impact of these factors may be necessary to lower the risk of AD.
“…Although the involvement of aluminium in neurodegenerative diseases remains controversial (Arsene and others ), several epidemiological studies have suggested that it produces toxicity in the central nervous, skeletal, and hematopoietic systems, causing problems such as osteomalacia, encephalopathy, dementia, and Alzheimer's disease (Malluche ; Frisardi and others ). It has been reported that exposures to aluminum concentration exceeding 0.11 mg/L in drinking water increase 1.5 times the risk of Alzheimer's disease in people aged 70 in comparison with intakes lower than 0.01 mg/L (Martyn and others ).…”
Aluminium is found naturally in foods and beverages, but levels increase notably during processing, packaging, storage, and cooking, as a consequence of its presence in food additives and the wide use of aluminium utensils and vessels. Dietary intake of Al was estimated in 2 population groups in southern Spain (families and university students) in a duplicate diet sampling study. Diets were sampled for 7 consecutive days, and Al was determined in acid-mineralized samples with electrothermal atomization-atomic absorption spectrometry (ETA-AAS). Mean values for Al intake were 2.93 and 1.01 mg/d in families and students, respectively, ranging from 0.12 to 10.00 mg/d. Assuming an average adult weight of 60 kg, the mean dietary exposures to aluminium were 0.34 and 0.12 mg/kg body weight/week in these groups, which amounted to 17% and 6% of the 2 mg/kg body weight estimated as the tolerable weekly intake by the Joint FAO/WHO Expert Committee on Food Additives. Bioaccessibility of dietary Al tested with in vitro studies ranged from 0.30 to 17.26% (absorbable fraction). The highest aluminium intakes were observed in subjects consuming diets with a low adherence to the Mediterranean diet, which were associated to high consumption of processed and canned food. On the contrary, subjects consuming diets with a high adherence to the Mediterranean diet patterns showed the lowest Al intakes. The present findings are useful for giving both a reliable estimate of total aluminium dietary intake and tolerable intake levels according to usual dietary habits.
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