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Dementia Among Asians: What’s Behind the Growing Cases?

admin — Tue, 11 Feb 2025 09:43:27 +0000

Dementia is a significant concern in Asia, with the highest number of cases reported in the region. Asia is currently reporting the highest number of dementia cases, with 22.9 million individuals affected, which is more than double the number reported in Europe at 10.5 million. ¹

In 2015, approximately 23 million people in the Asia-Pacific region were estimated to have dementia.²The estimated numbers of people with dementia by region are as follows: South Asia (6.96 million), Southeast Asia (3.55 million), and Asia (24.28 million).³Among Asian regions, East Asia has the highest estimated number of persons with Aβ-positive AD dementia (6.6 million), followed by South Asia (3.9 million).⁴

What is Aβ-positive AD dementia

Aβ-positive AD dementia refers to Alzheimer’s disease (AD) dementia, defined by the presence of β-amyloid (Aβ) plaques in the brain.

Recent studies on dementia causes, factors in Asia

Metabolic dysfunction plays a critical role in dementia risk.⁵Research indicates that Korean Americans may have a higher risk for Alzheimer’s due to lifestyle factors like alcohol consumption.⁶ Moreover, hypertension, dyslipidemia, obesity, and diabetes are more prevalent in minority ethnic groups compared to White people, with hypertension having a 1.57 times greater impact on dementia risk in South Asian people.⁷

The impact of hypertension, obesity, diabetes, low HDL, and sleep disorders on dementia risk was increased in South Asian people compared to White people.⁸ Furthermore, one in three Asian patients has the tau protein in the brain, a known risk factor for dementia.⁹

On the same note, it has been found that some Asian urban areas show higher prevalence rates of dementia (14.6%) and mild cognitive impairment (35.3%) compared to Europe. ¹⁰There is a high risk of under detection of cognitive impairment, delayed diagnosis, and suboptimal management of dementia among Asian Americans. ¹¹

Likewise, studies suggest a greater vascular contribution to dementia among South Asian adults, complicated by varying genetic risks.¹²

Main risk factors for dementia in Southeast Asia

The main risk factors for dementia vary across different regions in Asia, influenced by factors such as lifestyle, genetics, and access to healthcare. Several studies indicate a rising trend of dementia and cognitive impairment in Asia, aligning with patterns observed in Western countries. ¹³

In Southeast Asia, dementia of the Alzheimer’s type is the most common diagnosis, followed by vascular dementia and frontotemporal dementia. A study in Singapore found that younger patients with dementia and higher lifespan education, as well as older patients with moderate-to-severe cerebrovascular disease, experience a steeper decline in cognition.¹⁴

An Asian diet for healthy brain

Lifestyle significantly impacts dementia rates among Asian populations, with factors like diet, physical activity, social engagement, and smoking playing significant roles.

Asians love food. Asian cuisine offers a wide range of flavors and ingredients, with many dishes rich in vegetables, fish, and spices known for their health benefits. Traditional meals like steamed fish, tofu, and stir-fried greens provide essential nutrients that support brain health.

However, some recipes can be high in refined carbs, sodium, and unhealthy fats, such as deep-fried snacks and heavily processed foods. To maintain a healthy brain, Asians should be mindful of their diet, choosing nutrient-dense options while limiting excessive salt, sugar, and unhealthy oils.

Traditional Asian diets, characterized by high consumption of fruits, vegetables, and fish, along with herbs and spices like turmeric, are linked to a lower risk of dementia.¹⁵

Healthy diets such as the Mediterranean, DASH, and MIND diets are considered more effective in preventing dementia compared to the traditional “Western diet,” which is high in red meat and fats, and low in vegetables and fish. ¹⁶

Related: DASH Diet For Hypertension

A pro-oxidant, pro-inflammatory state is characteristic of aging and age-related degenerative diseases, so foods with anti-inflammatory effects or antioxidants may be effective in preventing dementia.¹⁷

References
1. https://www.thelancet.com/

2. https://www.alzint.org/

3. https://journals.sagepub.com/

4. https://www.alzint.org/

5. https://www.sciencedirect.com/

6. https://www.webmd.com/

7. https://pmc.ncbi.nlm.nih.gov/

8. https://www.thelancet.com/

9. https://www.straitstimes.com/

10. https://pmc.ncbi.nlm.nih.gov/articles/PMC11544519/

11. https://pmc.ncbi.nlm.nih.gov/articles/PMC8638681/

12. https://www.sciencedirect.com/

13. https://pmc.ncbi.nlm.nih.gov/articles/PMC11544519/

14. https://alzres.biomedcentral.com/

15. https://www.sciencedirect.com/

16. https://pmc.ncbi.nlm.nih.gov/articles/PMC9805113/

Alzheimer’s disease progression can be detected through the retina

admin — Thu, 13 Jul 2023 05:33:13 +0000

It is often said that the eyes are the windows to the soul. However, current research indicates that the eyes might also serve as windows for health issues.

According to an NIA-funded study, several changes in the brain that occur during Alzheimer’s disease can appear in the retina – a layer of tissue located at the back of the eye that contains specialized cells called photoreceptors, which are responsible for capturing light and initiating the visual process.

The retina can be affected by a variety of eye illnesses and diseases, including retinal detachment, macular degeneration, and diabetic retinopathy. Regular eye exams and early medical intervention are critical for maintaining retinal health and keeping healthy vision.

The findings, published in Acta Neuropathologica, provide information on the effects of Alzheimer’s disease on the retina and imply that noninvasive methods of retina monitoring could be used to consistently detect and track the condition.

Previous research has discovered symptoms of Alzheimer’s disease in the retina, such as amyloid protein accumulation and tissue thinning. Researchers at Cedars-Sinai Medical Center in Los Angeles examined donated postmortem retina and brain tissue from 86 people to better understand how these alterations in the retina connect to the evolution of Alzheimer’s.

The researchers discovered that amyloid deposits in the retina were five times greater in people with mild cognitive impairment (MCI) and nine times higher in patients with Alzheimer’s disease as compared to cognitively unimpaired people. The deposits were also unevenly distributed across the retina in all cases. The majority were discovered in the inner layers and parts of the retina involved in peripheral vision.

People with Alzheimer’s had larger amounts of amyloid plaques in their retinas than those with MCI. Furthermore, the researchers discovered that retinal abnormalities were associated with the severity of brain changes. These findings imply that amyloid deposits in the retina increase with Alzheimer’s disease progression and could be utilized to diagnose the condition early.

According to the Alzheimer’s Association, Alzheimer’s disease is caused by a combination of factors, including age, genetics, lifestyle, and environment. Other risk factors include traumatic brain injury, as well as heart and brain health. Conditions that harm the heart and blood arteries, such as heart disease, diabetes, stroke, high blood pressure, and high cholesterol, appear to increase the chance of developing vascular dementia.

The researchers then examined the retina tissue for the presence of microglia and other nervous system immune cells. Microglia aid in the removal of cellular waste such as amyloid plaques. The researchers discovered an increase in the number of microglia in MCI and Alzheimer’s retinas, but the fraction of these active in clearing away amyloid plaques was lower than in cognitively unimpaired brain samples. This shows that these retinal microglia may not be operating properly, as occurs in Alzheimer’s patients’ brains, and may contribute to the formation of amyloid deposits over time.

The researchers analyzed the proteins present in the retinas and brain tissue of donors with Alzheimer’s to those with normal cognition to assess the effects of Alzheimer’s on cellular processes in the retina. They discovered that in the brains and retinas of Alzheimer’s patients, proteins implicated in inflammation and neurodegeneration were activated, whereas those involved in cellular energy production and light perception were suppressed. These findings suggest that the retina may “mirror” the brain alterations linked with Alzheimer’s disease.

Sources: National Institute on Aging
Alzheimer’s Association

Delaying Alzheimer’s disease onset with a protein derived from corn

admin — Thu, 05 May 2022 11:26:09 +0000

Scientists at the University of Kansas (KU) have engineered an antigen using a protein from corn to combat the toxic buildup of proteins associated with Alzheimer’s disease (Alzheimer’s). This antigen could feasibly be used in potential immunisation approaches for Alzheimer’s – the antigen has been shown to induce an immune response and improve memory in mice with the disease.

A team led by Jackob Moskovitz, Associate Professor of Pharmacology & Toxicology at the KU School of Pharmacy, used a recombinant methionine (Met)-rich protein derived from corn to produce an antigen rich in methionine sulfoxide (MetO). The corn-based antigen, when injected to the body, goads the immune system into producing antibodies against MetO-containing proteins, including the MetO component of beta-amyloid, a protein toxic to brain cells that is associated with Alzheimer’s.

In research published in 2011, Moskovitz showed that immunising mice with the antigen could protect brain cells from amyloid-related toxicity and reduce the buildup of plaques. According to Moskovitz, there was also a roughly 50% improvement in the memory of immunised mice.

In addition, the study showed the antigen-injected mice exhibited better long memory capabilities, reduced beta-amyloid levels in both blood-plasma and the brain, as well as “reduced beta-amyloid burden and MetO accumulations in key brain regions.”

Moskovitz suggests such an immunisation be given to people as the risk of Alzheimer’s disease increases later in life, “around the time people are told to go get a colonoscopy for the first time in their 50s or 60s,” with further booster shots to maintain effectiveness.

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Iron build-up in the brain linked to age-related cognitive decline

admin — Thu, 03 Feb 2022 07:25:43 +0000

The accumulation or iron in the brains of aging organisms is said to contribute to neurodegenerative diseases including Alzheimer’s disease. According to researchers at Northwestern University Feinberg School of Medicine (Northwestern), treatment with drugs called iron chelators could combat neurodegenerative diseases and restore normal iron metabolism in those experiencing high iron levels.

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In a study of young and old mice, Northwestern researchers found the brain was the only organ which showed an increase in cellular iron concentrations as the animals aged.

“There is tight regulation of iron homeostasis (metabolism) in the brain, but it appears that this regulation is disrupted as we age,” said Professor Dr. Hossein Ardehali, Division of Cardiology and Pharmacology, Northwestern.

A colleague of Dr. Ardehali’s later discovered the upregulation of iron in key brain areas relating to cognition was due to increased production of the protein hepcidin in the brain. Hepcidin, in turn, was found to inhibit the activity of a protein called ferroportin, which helps regulate neuronal iron levels.

In short, the increased production of hepcidin and decreased activity in ferroportin results in heightened iron concentrations within the brain. It has also been established that heightened iron concentrations within the brain can induce oxidative damage and enhance cell death.

A possible therapeutic strategy is the use of iron chelators – substances that bind to iron and make it biologically unavailable — to treat iron accumulation in the brain, said Dr. Ardehali. Iron chelators are as yet unable to cross the blood-brain barrier, however, there is an ongoing clinical trial assessing the effects of a specific iron chelator that can cross the barrier, in Parkinson’s disease.

Different risks of overactive bladder with different dementia medications

admin — Mon, 10 Jan 2022 10:02:12 +0000

Some drugs taken to ease the symptoms of Alzheimer’s disease and dementia has been found to instead cause increased risk of overactive bladder (OAB) in patients. The class of drugs known as cholinesterase inhibitors (ChEI), are said to increase communication between nerve cells to enhance cognition and include donepezil, galantamine and rivastigmine, according to researchers from the University of Houston College of Pharmacy, US.

The study examined 524,975 adults (aged 65 and older) with dementia who were users of ChEIs (donepezil 80.72%, rivastigmine 16.41%, galantamine 2.87%). The primary outcome of interest was OAB diagnosis or prescription of antimuscarinics, drugs which help correct overactive bladder, within six months of ChEI initiation.

“[The study] found that the risk of overactive bladder varies across individual ChEIs,” elaborated Professor Rajender R. Aparasu, Department of Pharmaceutical Health Outcomes and Policy. “Using a national cohort of older adults with dementia, we also found that donepezil was associated with a 13% increased risk of OAB compared to rivastigmine, whereas there was no differential risk of OAB with galantamine and rivastigmine.”

“The findings suggest the need to understand and manage medication-related morbidity in older adults with dementia.”

[Dementia is a group of symptoms associated with a decline in memory, reasoning or other thinking skills of which Alzheimer’s disease is a common cause, accounting for 60%-80% of cases.]

Read: Oxygen production/expenditure may be key to Alzheimer’s treatment

Certain personality traits linked to Alzheimer’s disease and dementia

admin — Wed, 13 Oct 2021 10:11:22 +0000

Two distinct personality traits predict the accumulation of pathology associated with dementia, say researchers from the Florida State University (FSU) College of Medicine, US: neuroticism, which measures a predisposition for negative emotions; and conscientiousness, which measures the tendency to be careful, organised, goal-directed and responsible.

The research combined data from 3,000 participants from the Baltimore Longitudinal Study of Aging (BLSA) and previously published work in a meta-analysis that summarised 12 studies on personality and Alzheimer’s disease neuropathology. Personality was measured using a five-factor personality test, the most common personality assessment tool. At the time of their enrollment in the BLSA neuroimaging sub-study, all participants were free of dementia or other severe medical conditions.

Advances in brain scan technology made it possible to assess in vivo amyloid and tau neuropathology as well (researchers previously measured amyloid and tau in the brain through autopsy).

FSU’s latest study provides more robust estimates of the associations between personality and Alzheimer’s than older studies that only looked at the clinical diagnoses related to the condition – researchers found that participants who scored higher in neuroticism and lower in conscientiousness harbored more amyloid and tau deposits (the proteins responsible for the plaques and tangles that characterise Alzheimer’s).

The researchers also found risk associations to be stronger in studies of cognitively normal people compared to studies that included people with cognitive problems.

The findings suggest that personality can help protect against Alzheimer’s and other neurological diseases by delaying or preventing the emergence of neuropathology for those strong in conscientiousness and low in neuroticism.

“…low neuroticism helps with managing stress and reduces the risk of common mental health disorders. Similarly, high conscientiousness is consistently related to healthy lifestyles, like physical activity,” said Antonio Terracciano, professor of geriatrics at FSU.

“Over time, more adaptive personality traits can better support metabolic and immunological functions, and ultimately prevent or delay the neurodegeneration process.”

Concerns arise over possible link between COVID-19 and Alzheimer’s disease

admin — Thu, 09 Sep 2021 10:44:31 +0000

Experts warn that COVID-19 could have a “long-term impact” on the nervous system of patients, manifesting in a higher incidence of Alzheimer’s disease (Alzheimer’s) especially among the younger age groups. Although there are no molecular traces of SARS-CoV-2, the virus that causes COVID-19, in the brain, the nervous system symptoms of the virus are nonetheless associated with biomarkers for brain diseases and injuries. The perturbations associated with the virus were even found to reside in genetic variants associated with schizophrenia, depression, and other conditions.

Alzheimer’s involves a progressive mental decline, including severe memory loss and eventual loss of self – it has no cure.

According to medical experts, around 25% to 45% of those who died from COVID-19 are estimated to have suffered from Alzheimer’s, besides takingdamage to the lung, liver,and heart.

As the rate of mental illness climbs significantly in COVID-19 patients, there is significant need for preparedness for waves of Alzheimer’s cases in the future. Alzheimer′s Disease International (ADI), an international federation of Alzheimer’s and dementia associations across 100 countries, is one such organisation to have dedicated a team to further study the link between the coronavirus and dementia.

Brain metabolism cause of neurodegeneration in Alzheimer’s disease

admin — Tue, 27 Jul 2021 08:27:13 +0000

Alzheimer’s Disease (AD), the most common type of dementia, causes the death of neurons and leads to shrinking of the brain. Patients with AD will eventually experience gradual deterioration in memory, thinking, behaviour and the ability to perform everyday activities. Yet, scientists do not fully understand what causes this disease.

A recent research, conducted by a team from the School of Life Sciences at The Chinese University of Hong Kong (CUHK), suggests that early changes in brain metabolism may explain the neurodegeneration. The research team is the first to discover that a special gene variant causes astrocytes of the brain to exhaust the primary substance for neurotransmission, amino acids. The long term insufficiency of amino acids may result in compromised neurotransmission and hence cognitive and memory impairments. Findings also indicate that direct brain supplement of the missing amino acids was effective in alleviating the neurodegenerative outcomes as well as the functional degeneration.

These findings lay the groundwork for developing novel and targeted nutrition-centric disease-modifying therapeutic strategies. The research paper has been published in Advanced Science, a prestigious scientific journal.

According to the World Health Organization statistics published in 2020, around 50 million people are suffering from dementia worldwide and there are nearly 10 million new cases every year, in which AD is the most common form of dementia, contributing to 60-70% of cases.

While the predominant approach towards AD treatments has targeted beta-amyloid — the classic pathology of AD, the repeated failures of clinical trials of anti-amyloid therapies highlights the pressing need to identify novel molecular targets that may underlie AD pathogenesis. Recently, a growing body of evidence has hinted that AD is a pervasive metabolic disorder in which altered cellular fuel metabolism occurs at the early prodromal stages of the disease long before the symptoms manifest. Therefore, understanding how perturbations in metabolism are related to this prodromal stage is critical to identifying targets for disease-modifying therapies.

A previous study suggested an association between a synonymous single nucleotide polymorphism (SNP) in LRP6 gene and AD. In this study, the team found that this SNP is indeed correlated with diminished LRP6 gene expression in the forebrain region and the gene is predominantly expressed in astrocytes—the metabolic workhorses in the brain. By means of genetic deletion of LRP6 specifically in these cells within the adult forebrain of mice, both their cognitive and memory function were dramatically impaired. This phenotype is associated with extensive metabolic reprogramming occurring in the brain microenvironment.

Professor Kim Hei-Man Chow, Principle Investigator of this study and Assistant Professor of the School of Life Sciences, CUHK explained, “Findings show that the correct partitioning of fates of various metabolites is critical for maintaining the normal synaptic function in the brain. In normal situations, LRP6 drives a metabolic programme which facilitates astrocytes to utilise glucose as its major fuel source for energy production. In the absence of LRP6 function, the entire metabolic landscape in astrocytes is rewired, rendering them unable to utilise glucose but glutamine, an amino acid which is also a neurotransmitter released by neurons, together with branched chain amino acids (BCAAs) as fuel. This shift in metabolic dependence not only resulted in impaired brain glycolytic capacities but also exhausted amino acids that are essential for neurotransmitter recycling and synthesis. When this situation was manifested chronically, this consequently hampered synaptic fidelity which is the molecular basis of normal cognitive and memory functions.”

The metabolic changes do not only affect people who harbour the gene polymorphism at LRP6 locus but are also relevant to those having the genetic variant of the apolipoprotein E (APOE) E4 allele, the most common genetic risk factor of AD [Around 6.3-9.3% frequency in Asian (including Chinese) populations]. The research team found that protein product of the APOE-E4 allele hampers the normal functioning of LRP6 protein by trapping it inside the cell, keeping it away from the cell surface where it carries out its functions.

With recent advances in the field suggesting that brain metabolic dysfunction is at the core of Alzheimer’s disease, targeting the new metabolic need of the brain may become a potential strategy to manage the disease progression. The research team revealed that direct brain supplement of the missing glutamine and BCAAs was effective in alleviating the neurodegenerative outcomes as well as the functional degeneration.

Professor Chow added, “Specific nutrient supplementation is nowhere a new concept in clinics. Glutamine is supplemented clinically to patients with critical illness. On the other hand, all BCAAs are by default essential amino acids, and their oral supplements have been used with good tolerance in treatments of several neurologic diseases, including bipolar disorder, tardive dyskinesia, amyotrophic lateral sclerosis, and spinocerebellar degeneration. These clinical applications indicated that both glutamine and BCAAs can be consumed in considerable amounts by humans without adverse effects, and in many cases, with significant benefits. Together, our findings support that, in addition to traditional drug-based therapies, the adjunct nutrient-based approach has great potential for managing neurodegenerative disorders.”

This study was performed in collaboration with Professor Kwan Kin-Ming from the School of Life Science and Professor Ronald P Hart from the Rutgers University, US. The project was supported by the General Research Fund, Collaborative Research Fund, Alzheimer’s Association Research Fellowship and the School of Life Sciences Start-up Funding.

Poor sleep can accelerate progression of Alzheimer’s

admin — Mon, 21 Dec 2020 06:19:06 +0000

Disrupted sleep can accelerate the progression of Alzheimer’s disease, say scientists from the Washington University School of Medicine (WUSM). The scientists have identified a brain protein regulated by the natural sleep cycle, or circadian rhythm that accelerates the accumulation of toxic amyloid plaques associated with the inflammatory disease.

The brain protein in question is called YKL-40: high levels of it have been found in the cerebrospinal fluid of those suffering from the Alzheimer’s disease; these levels rise as the disease progresses.

“The gene for YKL-40 came up (during screening) as highly regulated by clock genes,” said Erik Musiek, WUSM associate professor of neurology. “That was really interesting because it is a well-known biomarker for Alzheimer’s.”

Further investigation into the correlation between YKL-40 and Alzheimer’s disease demonstrated that the circadian rhythm controls how much YKL-40 is produced.“If you have inflammation in the morning, you might get lots of YKL-40; if you get inflammation in the evening, when the clock’s in a different phase, you might get less YKL-40.”

The WUSM scientists also studied genetically modified mice lacking the gene for YKL-40 and found that these mice featured more microglia as they aged – microglia are protective immune cells that surround and prevent amyloid plaques from spreading.

Read: US study links poor sleep to reduced memory performance in seniors

“This YKL-40 protein probably serves as a modulator of the level of microglial activation in the brain,” Musiek added. “When you get rid of the protein, it appears the microglia are more activated to eat up the amyloid. It’s a subtle thing, a tweak in the system, but it seems to be enough to substantially reduce the total amyloid burden.”

The scientists then examined this idea in human subjects, drawing on genetic data on 778 subjects from aging and dementia studies and finding only a quarter of them featured a genetic variant that lowers levels of YKL-40; cognitive function declined 16% more slowly in that group.

“If your circadian clock is not quite right for years and years – you routinely suffer from disrupted sleep at night and napping during the day – the cumulative effect of chronic dysregulation could influence inflammatory pathways such that you accumulate more amyloid plaques.

“We hope that a better understanding of how the circadian clock affects YKL-40 could lead to a new strategy for reducing amyloid buildup in the brain.”

Detecting Alzheimer’s disease through blood test shows real potential

admin — Thu, 03 Dec 2020 05:56:05 +0000

A new blood test is able to check if those with mild memory loss are at risk of developing Alzheimer’s disease (AD) later on. AD is notoriously difficult to diagnose until much too late, so scientists at Sweden’s Lund University looked at ways to pick up the disease during its early stages, before it develops into dementia.

Their search focused on two proteins in the blood called phosphorylated tau and neurofilamet light, which have both featured as part of AD blood testing technologies. Analysing the levels of these two proteins in the blood of 573 subjects with memory loss helped the scientists build a revolutionary online tool; it incorporates data like age, gender and results from cognitive tests and combines them with results from the blood test to predict more accurately the risk of developing AD within two years or four years.

“Many people with AD seek care when they have only developed mild memory impairment, meaning many years before the dementia stage of the disease,” said the university’s professor of neurology Oskar Hansson, who led the research.

Read: New blood test for early-stage Alzheimer’s disease detection 100% accurate

“It is often difficult for doctors to give the correct diagnosis in people with mild memory impairment, as many different conditions other than AD can be the cause – our goal […] has been to find simple methods that can be used in primary care to make an early diagnosis and to begin treatment to relieve symptoms at an earlier stage.” While promising, the tool is currently only intended for use in research.