Dementia is a progressive, complex, irreversible neurodegenerative disease with wide-ranging effects on the affected individuals, carers and society. It is characterized by memory failure, loss of acquired skills resulting in apraxia, agnosia, emotional disturbances and interpersonal and social deterioration. The most common forms are Alzheimer’s Disease (AD) (75% of cases), Lewy body disease and vascular dementia (VaD). Mixed forms often co-exist(WHO2019).
Contributory risk factors for developing AD include: age(guerreiro2015,mendiola-precoma2016), genetic factors(buc2009,cedazo2007,farrer1997,Gomez-isla2009,kim2009,myers2008,liu2013,strittmatter1993), family history(green2002,silverman2005), midlife hypertension(LeeDC2012), obesity(LeeIM2012,LeeDC2012), diabetes(Thomas2006,LeeIM2012) and hypercholesterolemia(bendlinetal2010,Mann2014,LeeDC2012).
The apolipoprotein (APOE) ?4 allele is a genetic risk factor for AD and dementia(Chen2009Liu2013,Mendiola-precoma2016)): female carriers have a greater risk(Altman2014,Farrer1997,bretsky1999,damoiseaux2012). Carrying two ?4 alleles raises AD risk fivefold(Elbaz2007). Carriers have: decreased connectivity, small hippocampal volume(Wang2015) (a region highly affected by dementia pathology); higher brain beta-amyloid plaque density(Murphy2013) and more rapid brain neurodegeneration(Chiang2011,hostage2014,kimm2015) making carriers more susceptible to developing dementia.
Physical activity (PA) is considered protective against cognitive decline via multiple physiologic mechanisms, which provide neuroprotective and neuroplastic effects on brain structures(kirk-sancesmcgough2014) including brain neurochemistry(lista2010), increased cerebral blood flow(Rogers1990), increased production of neurotrophic factors(Huang2014), increased neurogenesis and neuronal plasticity, enhanced neuronal survival(colcombe2005) and decreased risk of cerebrovascular and cardiovascular disease (CVD)(blumentahal1991).
There are an estimated 46.8 million people with dementia worldwide (Princemwimoaguerchinternwordalszrepor2015p1-87) and nearly 10 million new cases annually, with projections of 152 million by 2050(who2015executivesummaryone).
There were an estimated 850,000 dementia sufferers in the UK in 2015, which is expected to rise to >1 million by 2025(alz2014bmabenbow2016). AD affects approximately 5-7% of the population aged ?60 years(Prinebrrycealbanses2013). In 2014, the annual cost of dementia to the NHS, local authorities and families was estimated to be ?26.3 billion from direct medical and social care costs and informal care (LewisFDementiaUKupdare2014al’ssoc). With an aging population, this will reach ?55 billion in 2040 (PrinceMetal2014dementiaukupdate), constituting a growing health, economic and carer burden.
The current absence of a disease-modifying treatment for AD highlights the necessity for investigating non-pharmacological approaches, such as PA, as an adjuvant to other treatments (amyloid and tau-based therapeutics). PA reduces risk of CVD(Lee2012lavie2009,ahlskoggeda2011,bherererickson2013), diabetes(thomas2006coch), hypertension(colcombekramererickson2oo4,isaacs2007,conrenlissan2013), hypercholesterolemia(bakker2018) and obesity(leeetal2012) (each contributing to cognitive impairment)( warburton2006), so a literature review is therefore warranted to determine whether PA can prevent or delay onset of dementia/AD in populations with genetic susceptibility. Critically appraised results will be presented, findings discussed, conclusions drawn and implications for dementia/AD management considered.
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