Preventive Neurology

Age is a disease vs. Ageing as a natural biological process: have your say  #PreventiveNeurology #HealthyAgeing I have always cracked the joke 'that life is a sexually transmitted neurodegenerative disease with a 100% mortality' . This usually gets a mutated laugh until people start pondering the implications of the joke and realise that I am being serious. Evolution never designed, and selected, the human brain and nervous system to function much past 35 years of age. It is only relatively recently that life expectancy has increased with the requirement of our brains to function into old age. It is clear that when we measure cognitive function, and brain volume, it is all downhill from about 35 years of age. Those of us who are older than 35 notice the subtle cognitive impairments that increase with age and the gradual malfunction of our nervous systems. When last have you tried tight-rope walking? Your failing balance system is simply a reflection of the global rot t

The costs of modifying the course of Alzheimer's disease with a biological therapy are mind-blowingly large. #BrainHealth #PreventiveNeurology The perspective in this week's NEJM is a sobering reminder of why we need effective preventive strategies for Alzheimer's disease (AD). If we have to rely on Pharma to deliver expensive biological disease-modifying therapies (DMTs) to treat the disease it may end up costing society an extortionist amount of money.  As most people with AD rely on the state for their healthcare can society afford expensive DMTs for symptomatic AD? I am not sure we can. People with symptomatic AD have already lost too much brain and slowing progression of their AD at this stage may be too late to have an impact on their, and their family's, QoL. The other issue is cost-effectiveness; most people with AD (pwAD) are aged and not economically active and hence any DMT will have to be relatively cheap to pass NICE's cost-effective threshold

I predict a brave new world in which a significant proportion of the population will be receiving pharmacological interventions to optimise the ageing process. #BrainHealth #PreventiveNeurology The following study is a good example of the revolution that genomics has brought to the practice of medicine.  The discovery (2003) that gain-of-function mutations in the proprotein convertase subtilisin–kexin type 9 (PCSK9) gene causes autosomal dominant hypercholesterolaemia, and the identification (2005) of loss-of-function mutations in PCSK9 causing lower low-density lipoprotein (LDL) cholesterol levels, led to the PCSK9 pathway becoming a therapeutic target.  PCSK9 is a secreted serine protease that binds to the extracellular domain of the LDL receptor and targets the LDL receptor to the lysosomal compartment for degradation. PCSK9 prevents recycling of the LDL receptor to the cell surface, thereby attenuating LDL clearance. PCSK9 circulates in plasma, where it is closely associa

Preserving the population's cognitive capital will reduce the burden of dementia on Society. #BrainHealth #HealthyAgeing At the 2017 Association of British Neurologists (ABN) meeting in Liverpool, Professor Martin Rossor, in his ABN Medalist Lecture, made the point that at a population level we should be attempting to preserve Cognitive Capital . He was making a plea for public health officials to focus on ways to encourage the population to preserve their cognition, which in turn would help delay the onset of neurodegenerative diseases. This is exactly our thinking and what underpins the hypothesis that to reduce all-cause dementia we should be testing population level prevention strategies targeting simple things such as vascular comorbidities and lifestyle factors that are established risk factors for dementia, or are associated with the development of dementia.   What are the chances of this strategy working for Alzheimer's disease (AD) the commonest cause of dementia?

Can we prevent neurological disorders? #NewsSpeak £1.5m awarded to apply preventive medicine to brain disorders Queen Mary University of London (QMUL) will establish a new Centre for Preventive Neurology, thanks to £1.5m of funding from Barts Charity . Jack Cuzick QMUL Press release : The Centre will be the first of its kind in the UK and dedicated to researching how to prevent disorders that affect the brain and nervous system – specifically, dementia, Parkinson’s disease, and multiple sclerosis (MS). There are currently an estimated 800,000 people living with dementia in the UK, with the disease contributing to 11 per cent of deaths in the UK in 2015. MS affects approximately 100,000 people, costing UK society £1.4 billion per year, and the number of people with Parkinson’s is set to rise to 162,000 by 2020. Despite recent advances in research using animal models, the three disorders currently have no proven disease-modifying treatments in humans. Professor Jack Cuzick

Public Health vs. Sugar Lobby. Who will win in a world that is anti-science and fuelled by alternative facts? #PoliticalSpeak #SugarTax  A targeted sugar tax works. The study below in California shows that one year following implementation of the the US's first large sugar-sweetened beverages (SSBs) tax, prices of SSBs increased in many, but not all, settings, but more importantly SSB sales declined, and sales of untaxed beverages (especially water) rose.  What is now needed is to assess whether this SSB tax has an impact on the health of the population; i.e. does shifting people away from SSBs to 'healthy beverages' result in loss of weight and improvement in population health, i.e. less obesity and a lower incidence of the metabolic syndrome and diabetes. If yes, a sugar tax will ultimately reduce cardiovascular mortality and potentially all cause dementia later in life.  I suspect the US Corn Refiners Association and other bodies with vested interest in sugar wi

Should we redefine ageing as a disease? #BrainHealth #ProfG #HealthyAgeing Most of neurologists equate amyloid deposition in the brain with Alzheimer's disease (AD). This study questions this assumption and suggests that amyloid deposition is simply a part of normal ageing. Demographics, the APOE genotype and midlife dyslipidaemia was associated with amyloid deposition. In comparison obesity, smoking, diabetes, hypertension, and cardiac and metabolic conditions, but not intellectual enrichment, were associated with greater AD-pattern neurodegeneration.  These results in elderly individuals supports the hypothesis that tackling common lifestyle factors obesity, smoking, diabetes, hypertension, and cardiac and metabolic conditions could prevent, or at least, delay the onset of symptomatic AD and is consistent with the falling incidence of AD in both the Cambridge and Framingham cohort studies.  Please note that although the incidence (number of new cases per 100,000 people