The frequency and influence of dementia risk factors in prodromal Alzheimer's disease

Bos, Isabelle; Vos, Stephanie J.B.; Frölich, Lutz; Kornhuber, Johannes; Wiltfang, Jens; Maier, Wolfgang; Peters, Oliver; Rüther, E.; Engelborghs, Sebastiaan; Niemantsverdriet, Ellis; Roeck, Ellen Elisa De; Tsolaki, Magda; Freund‐Levi, Yvonne; Johannsen, Peter; Vandenberghe, Rik; Lleó, Alberto; Alcolea, Daniel; Frisoni, Giovanni B.; Galluzzi, Samantha; Nobili, Flavio; Morbelli, Silvia; Drzezga, Alexander; Didic, Mira; Berckel, Bart N.M. van; Salmon, Eric; Bastin, Christine; Dauby, Solène; Santana, Isabel; Baldeiras, Inês; Silva, Dina; Wallin, Anders; Nordlund, Arto; Coloma, Preciosa M.; Wientzek, Angelika; Alexander, Myriam; Novak, Gerald; Gordon, Mark Forrest; Wallin, Åsa; Hampel, Harald; Herukka, Sanna‐Kaisa; Scheltens, Philip; Verhey, Frans R.J.; Visser, Pieter Jelle

doi:10.1016/j.neurobiolaging.2017.03.034

Cited by 28 publications

(28 citation statements)

References 36 publications

(35 reference statements)

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“…Lobo et al 36 did not find less MMSE decline in light drinkers than in abstainers. Bos et al 37 recently reported increased risk of cognitive decline (non Alzheimer types) with increased alcohol. Others have found a protective effect of moderate alcohol use only in those not carrying the ApoE4 allele (a risk gene for late-onset Alzheimer’s disease) 38…”

Section: Resultsmentioning

confidence: 99%

Effects of drinking on late-life brain and cognition

Topiwala

Ebmeier

2017

Evid Based Mental Health

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Alcohol consumption is common in Western countries and has been increasing in older adults. Latest figures from Great Britain suggest 75% of those over 65 years drink, an increase from 71% 10 years ago. Chronic heavy intake is a well-established cause of brain atrophy and dementia, with a recent long-term prospective study from the USA reporting a doubling of the odds of later severe memory impairment in those with a history of an alcohol use disorder. Drinking of moderate amounts has been reported to be protective for brain health in a number of epidemiological studies, including some claims of possibly reducing dementia risk. Rigorous recent research has questioned this belief, with new evidence of harmful associations in moderate drinkers compared with abstainers. This has raised suspicion that reported protective effects of moderate drinking were due to confounding by socioeconomic class and intelligence. Clinicians should look out for cognitive impairment in heavy drinkers, considering that abstinence may induce a degree of clinical improvement. Discussions with patients regarding moderate drinking should be informed by recent research. Health benefits of moderate drinking at least for cognitive function are questionable, and if they exist are probably limited to one unit of alcohol daily with respect to other body systems. IntroduCtIonAlcohol use is widespread and increasing across the developed world. Latest figures suggest that 58% of the UK population is drinking in excess of existing safe limits, 1 with 5% men and 4% of women consuming hazardous amounts (>50 units (400 g) for men and >35 units (280 g) for women weekly). Drinking in women and older adults of both sexes has been increasing, 2 with the percentage of those >65 years drinking increasing from 71% to 75% between 2005 and 2016. Those over 65 years of age are now more likely than any other age group to have drunk on at least 5 days in the preceding week.1 Alcohol-related harm is estimated to cost England around £21 billion per year, with £3.5 billion to the NHS, £11 billion tackling alcohol-related crime and £7.3 billion from lost work days and productivity costs. Health concerns associated with alcohol use have focused on liver dysfunction and more recently cancer. The public are largely ignorant of the potential risks of drinking with regards to cognition, in contrast to widespread knowledge of effects on the liver.3 Recommended drinking guidelines have remained unchanged in the UK from 1987 until 2016. Safe limits for men were set at 21 units (168 g) and for women at 14 units (112 g) per week pre-2016. Recent evidence of associations with cancer risk 4 at lower doses prompted revision of UK government alcohol guidance to 14 units (112 g) for both sexes, but current US guidelines still suggest that up to 24.5 units (196 g) weekly is safe for men.This clinical review summarises established effects of chronic heavy drinking on brain and behaviour/cognitive function, as well as the poorly understood impact of moderate consumption. Impl...

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Section: Resultsmentioning

confidence: 99%

Effects of drinking on late-life brain and cognition

Topiwala

Ebmeier

2017

Evid Based Mental Health

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“…CSF samples from the SPIN cohort have contributed to several international multicenter CSF biomarker studies [34][35][36][37][38]. The SPIN cohort has contributed to the characterization of different CSF biomarkers such as b-site APP-cleaving enzyme activity [39,40], sAPP-b [6,39,41], neurofilament light chain [41], YKL-40 [6,39,[41][42][43], progranulin [44], a panel of synaptic proteins [45], and mitochondrial DNA [46] in different neurodegenerative diseases.…”

Section: Resultsmentioning

confidence: 99%

The Sant Pau Initiative on Neurodegeneration (SPIN) cohort: A data set for biomarker discovery and validation in neurodegenerative disorders

Alcolea

Clarimón

Carmona-Iragui

et al. 2019

A&D Transl Res & Clin Interv

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101

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Introduction The SPIN (Sant Pau Initiative on Neurodegeneration) cohort is a multimodal biomarker platform designed for neurodegenerative disease research following an integrative approach. Methods Participants of the SPIN cohort provide informed consent to donate blood and cerebrospinal fluid samples, receive detailed neurological and neuropsychological evaluations, and undergo a structural 3T brain MRI scan. A subset also undergoes other functional or imaging studies (video‐polysomnogram, 18F‐fluorodeoxyglucose PET, amyloid PET, Tau PET). Participants are followed annually for a minimum of 4 years, with repeated cerebrospinal fluid collection and imaging studies performed every other year, and brain donation is encouraged. Results The integration of clinical, neuropsychological, genetic, biochemical, imaging, and neuropathological information and the harmonization of protocols under the same umbrella allows the discovery and validation of key biomarkers across several neurodegenerative diseases. Discussion We describe our particular 10‐year experience and how different research projects were unified under an umbrella biomarker program, which might be of help to other research teams pursuing similar approaches.

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“…Some studies suggest that the majority of cognitively normal individuals have low densities of NFT [104] with Braak stages 1/2 being characteristic of cognitively normal individuals and higher stages of at least mild cognitive impairment (MCI), and there is also less astrocytosis and microglial reaction [41]. By contrast, Bouras et al [32] found that all non-demented cases had NFT in layer II of the entorhinal cortex and in sector CA1 of the HC. Moreover, in non-demented individuals, NFT were more numerous in medial temporal lobe (MTL) regions and in cortical association areas when a memory deficit was present suggesting NFT could be related to memory loss in non-demented individuals [70].…”

Section: Risk Factors Agementioning

confidence: 99%

Risk factors for Alzheimer’s disease

Armstrong¹

2019

367

238

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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.

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The frequency and influence of dementia risk factors in prodromal Alzheimer's disease

Cited by 28 publications

References 36 publications

Effects of drinking on late-life brain and cognition

Effects of drinking on late-life brain and cognition

The Sant Pau Initiative on Neurodegeneration (SPIN) cohort: A data set for biomarker discovery and validation in neurodegenerative disorders

Risk factors for Alzheimer’s disease

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