Category: Neurodegenerative Diseases

Categories : Ageing Neurodegenerative DiseasesTags :

HRT May Help Ward off Alzheimer’s in at-risk Women

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Older woman smiling
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Hormone Replacement Therapy (HRT) could help prevent Alzheimer’s Dementia among women at risk of developing the disease, according to a study published in Alzheimer’s Research and Therapy.

The study shows that HRT use is associated with better memory, cognition and larger brain volumes in later life among women carrying the APOE4 gene – the strongest risk factor gene for Alzheimer’s disease.

The research team found that HRT was most effective when introduced early in the menopause journey during perimenopause.

Prof Anne-Marie Minihane, from University of East Anglia, led the study in collaboration with Prof Craig Ritchie at the University of Edinburgh.

Prof Minihane said: “We know that 25% of women in the UK are carriers of the APOE4 gene and that almost two thirds of Alzheimer’s patients are women.

“In addition to living longer, the reason behind the higher female prevalence is thought to be related to the effects of menopause and the impact of the APOE4 genetic risk factor being greater in women.

“We wanted to find out whether HRT could prevent cognitive decline in at-risk APOE4 carriers.”

The research team studied data from 1178 women participating in the European Prevention of Alzheimer’s Dementia initiative, a study set up to record participants’ brain health over time.

The project spanned 10 countries and tracked participants’ brains from ‘healthy’ to a diagnosis of dementia in some. Participants were included if they were over 50 and dementia-free.

The research team studied their results to analyse the impact of HRT on women carrying the APOE4 genotype.

Dr Rasha Saleh, also from UEA’s Norwich Medical School, said: “We found that HRT use is associated with better memory and larger brain volumes among at-risk APOE4 gene carriers. The associations were particularly evident when HRT was introduced early — during the transition to menopause, known as perimenopause.

“This is really important because there have been very limited drug options for Alzheimer’s disease for 20 years and there is an urgent need for new treatments.

“The effects of HRT in this observation study, if confirmed in an intervention trial, would equate to a brain age that is several years younger.”

Prof Anne Marie Minihane said: “Our research looked at associations with cognition and brain volumes using MRI scans. We did not look at dementia cases, but cognitive performance and lower brain volumes are predictive of future dementia risk.”

Prof Michael Hornberger, from UEA’s Norwich Medical School, said: “It’s too early to say for sure that HRT reduces dementia risk in women, but our results highlight the potential importance of HRT and personalised medicine in reducing Alzheimer’s risk.

“The next stage of this research will be to carry out an intervention trial to confirm the impact of starting HRT early on cognition and brain health. It will also be important to analyse which types of HRT are most beneficial,” he added.

Source: University of East Anglia

Categories : Ageing Neurodegenerative DiseasesTags :

Hearing Loss Linked to Dementia Risk

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A nationally representative study published in JAMA found that older adults with greater severity of hearing loss were more likely to have dementia, but the likelihood of dementia was lower among hearing aid users compared to non-users.

The findings are consistent with prior studies showing that hearing loss might be a contributing factor to dementia risk over time, and that treating hearing loss may lower dementia risk.

“This study refines what we’ve observed about the link between hearing loss and dementia, and builds support for public health action to improve hearing care access,” says lead author Alison Huang, PhD, MPH, a senior research associate in the Bloomberg School’s Department of Epidemiology and at the Cochlear Center for Hearing and Public Health, also at the Bloomberg School.

Hearing loss is a critical public health issue affecting two-thirds of Americans over 70. The growing understanding that hearing loss might be linked to the risk of dementia, which impacts millions, and other adverse outcomes has called attention to implementing possible strategies to treat hearing loss.

For the new study, Huang and colleagues analysed a nationally representative dataset from the National Health and Aging Trends Study (NHATS). Funded by the National Institute on Aging, the NHATS has been ongoing since 2011, and uses a nationwide sample of Medicare beneficiaries over age 65, with a focus on the 90-and-over group as well as Black individuals.

The analysis covered 2413 individuals, about half of whom were over 80 and showed a clear association between severity of hearing loss and dementia. Prevalence of dementia among the participants with moderate/severe hearing loss was 61% higher than prevalence among participants who had normal hearing. Hearing aid use was associated with a 32% lower prevalence of dementia in the 853 participants who had moderate/severe hearing loss.

The authors note that many past studies were limited in that they relied on in-clinic data collection, leaving out vulnerable populations that did not have the means or capacity to get to a clinic. For their study, the researchers collected data from participants through in-home testing and interviews.

How hearing loss is linked to dementia isn’t yet clear, and studies point to several possible mechanisms. Huang’s research adds to a body of work by the Cochlear Center for Hearing and Public Health examining the relationship between hearing loss and dementia.

Source: Johns Hopkins Bloomberg School of Public Health

Categories : Neurodegenerative Diseases New Compounds and TreatmentsTags : 1 Comment

Alzheimer’s Drug Breakthrough Hailed as ‘Momentous’

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An 18-month randomised controlled trial of the new Alzheimer’s drug lecanemab has been hailed as “momentous” after encouraging Phase III trial results. The effects, while moderate, stand in contrast to virtually all other Alzheimer’s drug development efforts which have ended in failure.

According to the trial results published in the New England Journal of Medicine, lecanemab slows the rate of progression of Alzheimer’s by about 25%, though it is only really effective if the disease is caught early. Cognitive assessment scores as well as positron-emission tomography (PET) imaging of amyloid showed benefits.

This may be of great benefit to those who already know that they are already at risk of the disease, such as actor Chris Hemsworth who, at age 39, is taking a break from acting after he discovered that he has a high genetic risk of Alzheimer’s.

At present, the only FDA-approved drug to slow the progression of Alzheimer’s, Aduhelm, is of questionable benefit at best, is exorbitantly expensive and there has been an official probe into alleged irregularities in its approval process.

The 1975 trial participants were 50–90 years old with early Alzheimer’s disease (mild cognitive impairment or mild dementia due to Alzheimer’s disease) with evidence of amyloid on PET or by cerebrospinal fluid testing. Participants were randomised to receive intravenous lecanemab (10mg/kg of body weight every 2 weeks) or placebo.

The primary end point was the change from baseline at 18 months in the score on the Clinical Dementia Rating–Sum of Boxes (CDR-SB; range, 0 to 18, with higher scores indicating greater impairment). Key secondary end points included change in amyloid burden on PET, and on other cognitive impairment assessment scores.

 The mean CDR-SB score at baseline was approximately 3.2 in both groups. The adjusted least-squares mean change from baseline at 18 months was 1.21 with lecanemab and 1.66 with placebo. In a substudy involving 698 participants, there were greater reductions in brain amyloid burden with lecanemab than with placebo. Other cognitive assessments favoured lecanemab as well. Lecanemab resulted in infusion-related reactions in 26.4% of the participants and amyloid-related imaging abnormalities with oedema or effusions in 12.6%.

Categories : General Interest Neurodegenerative DiseasesTags :

‘Thor’ Actor Takes a Break from Acting after Alzheimer’s Gene Discovery

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Actor Chris Hemsworth. Credit: Gage Skidmore / Wikimedia Commons

Actor Chris Hemsworth has announced that he is stepping back from acting in order to focus on preventative measures for Alzheimer’s disease.

The 39-year-old star of ‘Thor’ told Vanity Fair that genetic testing had confirmed that he had two pairs of a gene, APOE4. which is highly predictive of developing Alzheimer’s. About one in four have a single copy while 2–3% carry two copies of the gene.

The reason APOE4 increases Alzheimer’s risk isn’t not well understood. The APOE protein helps carry cholesterol and other types of fat in the bloodstream. Recent studies suggest that problems with brain cells’ ability to process lipids may play a key role in Alzheimer’s and related diseases.

Lipid imbalances can impair many of a cell’s essential processes. This includes creating cell membranes, moving molecules within the cell, and generating energy.

Hemsworth had made the discovery while making the TV series ‘Limitless‘, in which he engages in a variety of activities to push the limits of his own body and mind and explores ways of extending the lifespan.

“My concern was I just didn’t want to manipulate it and overdramatise it, and make it into some sort of hokey grab at empathy, or whatever, for entertainment,” said Hemsworth. “It’s not like I’ve been handed my resignation.”

He emphasises that he is thankful at having made the discovery, as it has made him more appreciative of his life, and it now means he can now take steps to protect his health.

Fortunately, research suggests that there are lifestyle changes that may offer preventative effects for APOE4 carriers, such as reducing stress and getting regular exercise – though the latter is unlikely to be a problem for the already athletic actor. Dietary measures include various low-carbohydrate diets (including ketogenic diets), regular portions of oily fish, cruciferous vegetables and abstaining from alcohol.

Supplements with potential benefits include DHA, quercetin, resveratrol, vitamin D3, vitamin K2, B-vitamin complex and possibly lithium.

Categories : Neurodegenerative DiseasesTags :

Alzheimer’s Prions also Appear in Down Syndrome

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Plaques and neurons. Source: NIAH

The brains of people with Down syndrome develop the same neurodegenerative tangles and plaques associated with Alzheimer’s disease and they frequently demonstrate signs of the neurodegenerative disorder in their 40s or 50s. A new study in the journal PNAS shows that these tangles and plaques are driven by the same amyloid beta (Aß) and tau prions that they showed are behind Alzheimer’s disease.

Prions begin as normal proteins that become misshapen and self-propagate. They spread through tissue like an infection by forcing normal proteins to adopt the same misfolded shape. In both Alzheimer’s and Down syndrome, as Aß and tau prions accumulate in the brain, they cause neurological dysfunction that often manifests as dementia.

Tau tangles and Aß plaques are evident in most people with Down syndrome by age 40, according to the National Institute on Aging, with at least 50% of this population developing Alzheimer’s as they age.

The new study highlights how a better understanding of Down syndrome can lead to new insights about Alzheimer’s, as well.

“Here you have two diseases – Down syndrome and Alzheimer’s disease – that have entirely different causes, and yet we see the same disease biology. It’s really surprising,” said Stanley Prusiner, MD, the study’s senior author, who was awarded the Nobel Prize in 1997 for his discovery of prions.

Down syndrome is the most common neurodegenerative disease among younger people in the United States, while Alzheimer’s is the most common among adults.

Down syndrome occurs because of an extra copy of chromosome 21. Among the many genes on that chromosome is one called APP, which codes for one of the major components of amyloid beta. With an extra copy of the gene, people with Down syndrome produce excess APP, which may explain why they develop amyloid plaques early in life.

A clearer picture in young brain

It’s been known for some time that Aß plaques and tau tangles are present in both Down syndrome and Alzheimer’s. Having shown earlier that these neurodegenerative features are provoked by prions in Alzheimer’s, the researchers wanted to know whether the same aberrant proteins were present in the brains of people with Down syndrome.

While these plaques and tangles in the brains of people with Alzheimer’s disease have been well-studied, it can be challenging to discern which changes in the brain are from old age and which are from prion activity, said Prusiner.

“Because we see the same plaques-and-tangles pathology at a much younger age in people with Down syndrome, studying their brains allows us to get a better picture of the early process of disease formation, before the brain has become complicated by all the changes that go on during aging,” he said. “And ideally, you want therapies that address these early stages.”

Employing a variation on the novel assay they used in the Alzheimer’s study, the team looked at donated tissue samples from deceased people with Down syndrome, which they obtained from biobanks around the world. Of the 28 samples from donors aged 19 to 65 years old, the researchers were able to isolate measurable amounts of both Aß and tau prions in almost all of them.

New insights could yield preventative measures

The results confirm not only that prions are involved in the neurodegeneration seen in Down syndrome, but that Aß drives the formation of tau tangles as well as amyloid plaques, a relationship that has been suspected but not proven.

“The field has long tried to understand what the intersection is between these two pathologies,” said lead author Carlo Condello, PhD, also a member of the UCSF Institute for Neurodegenerative Diseases. “The Down syndrome case corroborates the idea; now you have this extra chromosome that’s driving the Aß, and there’s no tau gene on the chromosome. So, it’s truly by increasing the expression of Aß that you kick off production of the tau.”

These and other insights gained from studying the brains of people with Down syndrome will lead to a much better picture of how prions begin to form in the first place, said Condello.

Whether the Down syndrome brain tissue will prove to be the ultimate model for developing treatments for Alzheimer’s remains to be seen, the researchers said. While the two disorders share many similarities in their prion pathobiology, there are some differences that may be limiting.

Still, the researchers said, studying the plaques and tangles in Down syndrome is a promising route to identifying the specific prions that arise at the very earliest stages of the disease process. That insight could open new vistas on not only treating but perhaps even fending off Alzheimer’s disease.

“If we can understand how this neurodegeneration begins, we are one big step closer to being able to intervene at a meaningful point and actually prevent these large brain lesions from forming,” Condello said.

Source: University of California – San Francisco

Categories : Neurodegenerative DiseasesTags :

Nose Picking Opens up a Pathway for Dementia-linked Bacteria

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Photo by Ketut Subiyanto

In mice, researchers have shown that Chlamydia pneumoniae can travel through the olfactory nerve in the nose and into the brain, where it creates markers that are a tell-tale sign of Alzheimer’s disease. Damage from nose picking can make infection easier for C. pneumoniae.

The Griffith University study, published in the journal Scientific Reports, showed that C. pneumoniae used the nerve extending between the nasal cavity and the brain as an invasion path to invade the central nervous system. The cells in the brain then responded by depositing amyloid beta protein which is a hallmark of Alzheimer’s disease.

Professor James St John, Head of the Clem Jones Centre for Neurobiology and Stem Cell Research, is a co-author of the world first research.

“We’re the first to show that Chlamydia pneumoniae can go directly up the nose and into the brain where it can set off pathologies that look like Alzheimer’s disease,” Professor St John said. “We saw this happen in a mouse model, and the evidence is potentially scary for humans as well.”

The olfactory nerve in the nose is directly exposed to air and offers a short pathway to the brain, one which bypasses the blood-brain barrier. It’s a route that viruses and bacteria have sniffed out as an easy one into the brain.

The team at the Centre is already planning the next phase of research and aim to prove the same pathway exists in humans.

“We need to do this study in humans and confirm whether the same pathway operates in the same way. It’s research that has been proposed by many people, but not yet completed. What we do know is that these same bacteria are present in humans, but we haven’t worked out how they get there.”

There are some simple steps to look after the lining of your nose that Professor St John suggests people can take now if they want to lower their risk of potentially developing late-onset Alzheimer’s disease.

“Picking your nose and plucking the hairs from your nose are not a good idea”,” he said.

“We don’t want to damage the inside of our nose and picking and plucking can do that. If you damage the lining of the nose, you can increase how many bacteria can go up into your brain.”

Smell tests may also have potential as detectors for Alzheimer’s and dementia says Professor St John, as loss of sense of smell is an early indicator of Alzheimer’s disease. He suggests smell tests from when a person turns 60 years old could be beneficial as an early detector.

“Once you get over 65 years old, your risk factor goes right up, but we’re looking at other causes as well, because it’s not just age—it is environmental exposure as well. And we think that bacteria and viruses are critical.”

Source: Griffith University

Categories : Neurodegenerative DiseasesTags :

Best Evidence Yet That Lowering Blood Pressure Cuts Dementia Risk

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Old man
Source: JD Mason on Unsplash

A global study of over 28 000 people has provided the strongest evidence to date that lowering blood pressure in later life can cut the risk of dementia. The study, which included five randomised controlled trials, was published in the European Heart Journal, and constitutes the highest grade of evidence for this preventative association.

Dr Ruth Peters, Program Lead for Dementia in The George Institute’s Global Brain Health Initiative, said that with no significant dementia treatment breakthroughs being made, reducing the risk of developing the disease would be a welcome step forward.

“Given population ageing and the substantial costs of caring for people with dementia, even a small reduction could have considerable global impact,” she said.

“Our study suggests that using readily available treatments to lower blood pressure is currently one of our ‘best bets’ to tackle this insidious disease.”

Dementia is fast becoming a global epidemic, currently affecting an estimated 50 million people worldwide. This number is projected to triple by 2050 mainly from ageing populations.

Current estimates put the cost at US$20–$40 000 per person with the condition each year.

Dr Peters explained that while many trials have looked at the health benefits of lowering blood pressure, few included dementia outcomes and even fewer were placebo-controlled.

“Most trials were stopped early because of the significant impact of blood pressure lowering on cardiovascular events, which tend to occur earlier than signs of dementia,” she said.

To examine the relationship between blood pressure and dementia more closely, researchers analysed five double-blind placebo-controlled randomised trials that used different blood pressure lowering treatments and followed patients until the development of dementia. A total of 28 008 individuals with an average age of 69 and a history of hypertension from 20 countries were included. Across these studies, the mid-range of follow up was just over four years.

“We found there was a significant effect of treatment in lowering the odds of dementia associated with a sustained reduction in blood pressure in this older population,” said Dr Peters.

“Our results imply a broadly linear relationship between blood pressure reduction and lower risk of dementia, regardless of which type of treatment was used.”

Researchers hope the results will help in designing public health measures to slow the advance of dementia as well as informing treatment, where there may be hesitancy in how far to lower blood pressure in older age.

“Our study provides the highest grade of available evidence to show that blood pressure lowering treatment over several years reduces the risk of dementia, and we did not see any evidence of harm,” said Dr Peters.

“But what we still don’t know is whether additional blood pressure lowering in people who already have it well-controlled or starting treatment earlier in life would reduce the long-term risk of dementia,” she added.

Source: George Institute for Global Health

Categories : Metabolic Disorders Neurodegenerative DiseasesTags :

Link Found Between Dementia Indicators and Metabolism

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MRI images of the brain
Photo by Anna Shvets on Pexels

A world-first study published in the journal Diabetes, Obesity and Metabolism, has uncovered an association between metabolism and dementia-related brain measures, providing valuable insights about the disease.

Analysing UK Biobank data from 26 239 people, University of South Australia researchers found that those with obesity related to liver stress, or to inflammation and kidney stress, had the most adverse brain findings.

The study measured associations of six diverse metabolic profiles and 39 cardiometabolic markers, using MRI brain scan measures of brain volume, brain lesions, and iron accumulation, to identify early risk factors for dementia.

Participants with metabolic profiles associated with obesity were more likely to have adverse MRI profiles showing lower hippocampal and grey matter volumes, greater burden of brain lesions, and higher accumulation of iron.

UniSA researcher, Dr Amanda Lumsden, says the research adds a new layer of understanding to brain health.

“Dementia is a debilitating disease that affects more than 55 million people worldwide,” Dr Lumsden said.

“Understanding metabolic factors and profiles associated with dementia-related brain changes can help identify early risk factors for dementia.

“In this research, we found that adverse neuroimaging patterns were more prevalent among people who had metabolic types related to obesity.

“These people also had the highest Basal Metabolic Rate (BMR) -how much energy your body requires when resting in order to support its basic functions — but curiously, BMR seemed to contribute to adverse brain markers over and above the effects of obesity.”

Senior investigator Professor Elina Hyppönen said that the finding presents a new avenue for understanding brain health.

“This study indicates that metabolic profiles are associated with aspects of brain health. We also found associations with many individual biomarkers which may provide clues into the processes leading to dementia,” said Prof Hyppönen.

“The human body is complex, and more work is now needed to find out exactly why and how these associations arise.”

Source: University of South Australia

Categories : Neurodegenerative DiseasesTags : 1 Comment

Serious Infections Increase Alzheimer’s and Parkinson’s Risk

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Old man
Source: JD Mason on Unsplash

Infections needing hospitalisal treatment in early- and mid-life are associated with an increased subsequent risk of Alzheimer’s and Parkinson’s diseases, according to a population-based, case control study by published in PLOS Medicine. No such increase was seen for amyotrophic lateral sclerosis (ALS), however.

The study used Swedish data on individuals diagnosed with Alzheimer’s disease, Parkinson’s disease or ALS, from 1970–2016, as well as five matched controls per case. The analysis included more than 290 000 Alzheimer’s disease cases, 100 000 Parkinson’s disease cases and 10 000 ALS cases.

The results show that a hospital-treated infection five or more years before diagnosis was associated with a 16% increased risk of Alzheimer’s disease and a 4% higher risk of Parkinson’s disease. The associations only applied to individuals diagnosed before the age of 60, whereas no association was found for those diagnosed later in life.

Individuals with multiple hospital treatments for infections before age 40 was associated with the highest risk of disease, with more than doubled risk of Alzheimer’s disease and more than 40% increase in the risk of Parkinson’s disease.

No association was observed for ALS, regardless of age at diagnosis. Due to the observational nature of the study, no causal link could be established.

“These findings suggest that infectious events may be a trigger or amplifier of a pre-existing disease process, leading to clinical onset of neurodegenerative disease at a relatively early age,” said Jiangwei Sun, the study’s first author and postdoctoral researcher at Karolinska Institutet.

Source: Karolinska Institutet

Categories : Neurodegenerative DiseasesTags :

7 Lifestyle Habits may Reduce Dementia Risk in Diabetes

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Old man jogging
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A combination of seven healthy lifestyle habits including sleeping seven to nine hours daily, regular exercise and frequent social contact was associated with a lower risk of dementia in people with type 2 diabetes, according to a study published online in the journal Neurology.

“Type 2 diabetes is a worldwide epidemic that affects one in 10 adults, and having diabetes is known to increase a person’s risk of developing dementia,” said study author Yingli Lu, MD, PhD, of Shanghai Jiao Tong University School of Medicine in China. “We investigated whether a broad combination of healthy lifestyle habits could offset that dementia risk and found that people with diabetes who incorporated seven healthy lifestyle habits into their lives had a lower risk of dementia than people with diabetes who did not lead healthy lives.”

For the study, researchers looked at a health care database in the United Kingdom and identified 167 946 people 60 or older with and without diabetes who did not have dementia at the start of the study. Participants completed health questionnaires, provided physical measurements and gave blood samples. For each participant, researchers calculated a healthy lifestyle score of 0 to 7, with one point for each of 7 healthy habits. Habits included no current smoking, moderate alcohol consumption of up to one drink a day for women and up to two a day for men, regular weekly physical activity of at least 2.5 hours of moderate exercise or 75 minutes of vigorous exercise, and 7 to nine hours of sleep daily.

Another factor was a healthy diet including more fruits, vegetables, whole grains and fish and fewer refined grains, processed and unprocessed meats. The final habits were being less sedentary, which was defined as watching television less than four hours a day, and frequent social contact, which was defined as living with others, gathering with friends or family at least once a month and participating in social activities at least once a week or more often. Researchers followed participants for an average of 12 years. During that time, 4,351 people developed dementia. A total of 4% of the people followed only zero to two of the healthy habits, 11% followed three, 22% followed four, 30% followed five, 24% followed six and 9% followed all seven. People with diabetes who followed two or fewer of the seven healthy habits were four times more likely to develop dementia than people without diabetes who followed all seven healthy habits. People with diabetes who followed all of the habits were 74% more likely to develop dementia than those without diabetes who followed all the habits. For people with diabetes who followed all the habits, there were 21 cases of dementia for 7474 person-years, or 0.28%.

For people with diabetes who followed only two or fewer habits, there were 72 cases of dementia for 10 380 person years or 0.69%. After adjusting for factors like age, education and ethnicity, people who followed all the habits had a 54% lower risk of dementia than those who followed two or fewer. Each additional healthy habit people followed was associated with an 11% decreased risk of dementia. The association between healthy lifestyle score and dementia risk was not affected by medications people took or how well they controlled their blood sugar.

“Our research shows that for people with type 2 diabetes, the risk of dementia may be greatly reduced by living a healthier lifestyle,” Dr Lu said. “Doctors and other medical professionals who treat people with diabetes should consider recommending lifestyle changes to their patients. Such changes may not only improve overall health, but also contribute to prevention or delayed onset of dementia in people with diabetes.” A limitation of the study was that people reported on their lifestyle habits and may not have remembered all details accurately. Lifestyle changes over time were also not captured.

Source: American Academy of Neurology