Alzheimer’s disease is a progressive form of dementia which causes memory loss and an inability to carry out the simplest tasks. This usually begins in middle age but can affect people at any age. As Alzheimer’s progresses, someone with the condition might need 24 hour care. People with Alzheimer’s typically need long term care and support, and will eventually become completely dependent on others for their basic personal needs.
There are around 820,000 people living with dementia in the UK and one million people in care homes (Alzheimer’s Society, 2006). The economic cost of caring for these patients was estimated by the Department of Health to be £11 billion in 1997/98. Worldwide it is estimated that nearly 30 million people are living with dementia, and by 2015 the figures for those over 65 will have more than doubled in some countries. However Alzheimer’s is currently one of our most underfunded health problems.
There are many factors known to influence the likelihood of developing Alzheimer’s disease: there is a large genetic component; early age at which your mother had children; poor diet; lack of exercise and obesity.
Genes clearly play a large role in susceptibility to Alzheimer’s disease, but the picture is complex because genes influence our individual risk through both direct effects on brain cells (an expressed trait) and indirect effects on unknown environmental factors which then interact with the direct genetic effect, creating an ‘environmental’ effect (a polygenic risk).
There is evidence for such a polygenic susceptibility to Alzheimer’s disease, as there is a range of different markers all showing directly that genes contribute to the incidence of Alzheimer’s. Examples include the effects on age of onset in identical twins reared apart; studies with genetically engineered mice which have reduced levels of amyloid precursor; studies with genetically engineered mice which have increased amounts of amyloid and develop memory loss at an earlier age than normal mice (Cibelli et al., 2001); the finding that people from families in which there is a history of Alzheimer’s disease show more brain shrinkage on MRI scans than those from less affected families; and the finding that the drugs used to treat Alzheimer’s disease (cholinesterase inhibitors) have greater benefits for people with a family history of Alzheimer’s disease.
In parallel, there are also indirect studies which suggest that genes indirectly contribute to susceptibility to Alzheimer’s through polygenic effects on environmental factors. A good example of this is the effect of smoking on susceptibility to Alzheimer’s disease, which occurs more commonly in women with genetic variants linked to low vitamin B12 levels (Steinberg et al., 2000), and also in men who carry a variant associated with lower testosterone (Gutknecht et al., 1998).
Although these latter studies do not use genetic information alone, they are good evidence that genes interacting with the environment influence susceptibility to Alzheimer’s disease.
In order to build up a more complete picture of how genes contribute to risk and drug responses in patients with Alzheimer’s disease we need to make further progress in identifying genetic variants which contribute directly or indirectly through environmental effects to Alzheimer’s disease.
There are several types of gene which could be related to Alzheimer’s disease: those regulating the way in which amyloid precursor is produced or removed, those involved in breaking up and taking up amyloid, those involved in activating and inhibiting enzymes such as cholinesterase’s, or those which regulate the processes involved in maintaining cell structure and function.
Alzheimer’s is a devastating disease that can be prevented by making informed lifestyle choices.
It’s important to keep your mind and body active, eat healthy foods, maintain physical balance with exercise and reduce stress.
A recent study has revealed 11 gene variations that significantly increased the risk of Alzheimer’s, helping to better predict and understand this disease. The discovery was made by a team at Northwestern University Feinberg School of Medicine in Chicago, Illinois. They found that these variations are linked with B-amyloid peptide, which is thought to contribute to the formation of brain plaques that are a hallmark of Alzheimer’s.
The team also found that these genetic variations, or genes, increased the risk of getting late-onset Alzheimer’s disease more than early onset, but they did not seem to increase the risk for other dementias like Parkinson’s disease.
However, further investigation showed that these variations increased the risk of developing Alzheimer’s in people who were predisposed to diabetes and schizophrenia. More research is needed to fill in the gaps about the role of this gene variation, but understanding how they are linked helps us understand why certain individuals develop Alzheimer’s disease.
B-amyloid peptide is a neurotoxic protein found in the plaque deposits that build up between neurons and form a barrier to communication. As an individual ages, they are more likely to develop these plaques, which can interfere with many brain processes. B-amyloid peptide has been linked with Alzheimer’s for decades, but it wasn’t until recently that we understood how it affects people. Researchers are still working to determine what makes the gene variation increase Alzheimer’s risk, but this study is a huge leap into the future in terms of prediction and understanding for dementia patients.
The very exciting news is that prevention with lifestyle choices can help you stay out of the category of people who have this genetic variation. It’s never too late to make better choices for your health and reduce your risk of developing Alzheimer’s disease.
A similar study was conducted on a subset of participants from the Australian Imaging, Biomarkers & Lifestyle (AIBL) study at Neuroscience Research Australia, exploring the effect of intensive lifestyle intervention on genes associated with dementia risk. Participants were included in the study if they had a genetic variant (APOE4, APOE2, or APOLLO) that predisposes individuals to Alzheimer’s disease. The participants were grouped into two categories: those who underwent an intensive lifestyle intervention after being diagnosed with mild cognitive impairment (MCI), and those who were not exposed to the lifestyle intervention until they had been diagnosed with Alzheimer’s disease.
The results of this study, published in the January 2015 edition of Diabetes Care, showed that participants who underwent a better diet, regular exercise, and stress management training experienced a decrease in one specific gene variant, APOLLO, which is linked with higher risk of Alzheimer’s disease. The study also found that the participants who only underwent lifestyle interventions after being diagnosed with Alzheimer’s experienced an increase in other gene variants associated with Alzheimer’s disease. This shows that it can be possible to decrease your risk of this devastating disease by implementing healthier lifestyle choices before you are diagnosed, so it’s very important to implement small changes now.
The study also showed that the participants who lowered their risk of Alzheimer’s disease by 2 to 3 years after undergoing a two-year lifestyle intervention were able to retain this positive effect even after four years. Participants with high levels of a certain brain-derived peptide called amylin were able to extend their time in the “premium” category (reduced risk for Alzheimer’s) by up to three years. This suggests that lifestyle interventions can potentially delay Alzheimer’s disease symptoms, meaning you may be able to take advantage of this protective effect for even longer.
A similar study conducted by the Rush Alzheimer’s Disease Center of Chicago, Illinois followed 1,280 people who had been diagnosed with MCI between 2006 and 2012. Their results showed that participants who underwent an intensive lifestyle intervention program experienced a significantly greater cognitive improvement than those in a control group during the first year of treatment. These cognitive gains were maintained throughout the study’s five-year follow-up period, showing that a healthy lifestyle can help to maintain our brain health for longer than we previously thought.
The study was published in the April 2015 edition of Neurology , and it shows low levels of APOE4 gene variant among subjects undergoing intensive lifestyle improvement. This suggests that lifestyle modification can decrease the risk of Alzheimer’s disease even more than previously believed, and it also shows that you may be able to delay or possibly reverse symptoms of this devastating illness.
This is exciting news for anyone who has other genetic variants such as APOE2 or APOLLO which are linked to an increased risk of Alzheimer’s disease, as it demonstrates the ability to reduce your risk and create powerful changes in your brain health. The more life-changing lifestyle choices you make now, such as ditching processed foods for natural ones or working out regularly, the greater chance you have of living a long, healthy life free from Alzheimer’s disease.
MOST large genes are made up of clusters of smaller subunits. Researchers have now identified two regions in the human genome which might be implicated in Alzheimer’s disease because they contain many such gene clusters. If one fails to function properly it may cause Alzheimer’s.
The researchers, from the University of Oxford, found that these loci were particularly densely packed with genes involved in synaptic transmission – the process by which nerve impulses are passed between neurons (nerve cells). They suspect that if one of them goes wrong this might result in a diseased brain.
Dr David Lees and Professor Hugh Perry, who led the team, published their findings in the journal Genome Research . They said: “With these new results we have found two regions in which genes involved in Alzheimer’s disease may be located.”
Most of the large genes that contain clusters of individual genes are dubbed MACROBLOCKS: they contain up to 1,000 individual genes. While all the MACROBLOCS identified so far are believed to be involved in neuron-specific functions, some of them are also likely to be neurologically important.
The team found around half of the largest 25 genes (which are mostly neuro-developmental or neuronal) fall into the two MACROBLOCKS identified. The researchers said: “It is therefore possible that one or more of the genes in these loci are related to Alzheimer’s.“
The team used a technique called a chromosomal microdeletion assay (COMIDA) to search for regions of DNA sequence with large numbers of gene clusters. The Oxford team found that two MACROBLOCKS, A3 and B9, were particularly densely populated with genes involved in synaptic transmission.
The researchers said: “We propose that the genetic underpinnings of Alzheimer’s disease are likely to be complex, but we speculate that certain common elements may play a role.” They concluded: “MACROBLOCS may represent one such common element because they contain so many genes involved in synaptic transmission.”
Bottomline, our genetic makeup plays a vital role in being prone to having Alzheimer’s. So to mitigate the risks and/or prevent yourself from having that, be healthier!
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