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Alzheimer’s disease (AD) is the commonest cause of dementia in the world. It is a degenerative disease of the brain, which occurs due to shrinkage of different parts of brain. Symptoms include progressive loss of memory and other cognitive functions. It is more common in older people; however, it can occur in young too.

The number of people living with AD doubles every 5 years beyond the age of 65. Even though AD is more common in older people, one should note that normal ageing does not cause memory loss. In addition to advancing age, hereditary factors also play a role. Familial AD accounts for <1% of all cases of AD. The proportion of familial AD is higher in early onset (<60 years of age) AD.

Memory loss is the commonest symptom. People with AD may forget names of familiar people. They may forget where they have kept the things of daily use. Memory loss is more for recent events, and remote memory may remain intact until late stages of the disease. Those affected with AD lose the sense of direction and may not be able to reach known places. They can have difficulty in calculation, resulting in inability to do financial transactions.

Self-care is affected and they may need assistance for activities of daily living such as bathing, dressing, feeding and toileting needs. Some patients with AD can also have psychological symptoms such as depression, anxiety, confusion, irritability and sleep disturbances. The disease can deteriorate over time. In mild cases, people have only mild forgetfulness and may be able to carry out all activities by themselves. However, in severe cases of AD, people get bed-bound and depend on caregivers for even their basic daily needs.

AD is the commonest cause of dementia and there is no cure. However, there are several other causes of dementia, which can get cured with prompt initiation of treatment. These include vitamin B 12 deficiency, thyroid diseases, alcohol abuse, brain infections, brain tumours and head injury to name a few.

Brain scan should be done in all cases suspected to have dementia. It can detect strokes, bleeding and tumours in brain. In cases suspected to have brain infection, lumbar puncture (spinal tap) is useful. Blood test for vitamin B12 and D deficiency, thyroid disease and sugar should be done. Repeated episodes of low sugar (hypoglycaemia) can also cause dementia.

There is no cure for AD. Medicines are given to slow the progression of disease, and cause mild improvement in cognitive functions. In dementia caused by other diseases, the underlying cause can be treated and results are very pleasing.

Tips to prevent dementia and cognitive decline

1. Avoid stress
2. Sleep adequately (7-9 hours per night)
3. Engage in regular physical activity such as running, brisk walking, cycling or swimming (150 minutes or more per week)
4. Engage in brain exercises, such as solving crossword puzzles, Sudoku or learning a new skill
5. Eat healthy foods such as fruits, vegetables, whole cereals, blueberries, fish and dry fruits. Avoid fatty and ultra-processed packaged foods.
6. Keep BP, sugar and cholesterol within normal limits
7. Maintain normal body weight. Avoid overweight and obesity
8. Wear helmets and seatbelts while driving- to prevent head injury
9. Avoid smoking and alcohol abuse
10. Consult a Neurologist if you develop memory loss.

Also Read: Immunotherapy treatments are avoided by tumours by forming temporary structures: Study

India reported 4,510 new COVID cases in the last 24 hours with a daily case positivity rate of 1.33 per cent, according to the Ministry of Health and Family Welfare on Wednesday.

With this, the active cases in the country stand at 46,216. According to the Ministry, 5,640 COVID patients recovered from the disease in the last 24 hours taking the total number of recoveries in the country to 4,39,72,980.

The recovery rate currently is 98.71 per cent.

The weekly positivity rate stands at 1.80 per cent.

Under the nationwide vaccination drive, 12,27,054 COVID vaccines were jabbed in the last 24 hours.

Covid vaccine

The cumulative vaccine doses administered in the country so far reach to 216.95 crore.

Also Read: Govt to start network of regional BSL-3 labs to brace for future pandemics

The Indian government is aiming to establish four regional BSL-3 virology biosafety facilities, with ICMR-NIV Pune leading the initiative and research. Official sources told ANI that these facilities will function as regional labs, with ICMR-NIV Pune overseeing their research.

During a disease epidemic, it is critical to increase swift surveillance and guarantee early diagnosis, according to the sources. The centre lab will be in Jabalpur, the Northeast lab in Dibrugarh, the North lab in Mohali, and the South lab in Bangalore.

On September 27, President Droupadi Murmu is expected to lay the groundwork for one of the labs in Bangalore.

“These labs will be physical labs and will be useful for future preparedness if any disease outbreak or pandemic is reported in future as strengthening of lab infrastructure is crucial and will help spread and detection of virus faster. The project of these labs comes under the PM Ayushman Bharat Health infrastructure Mission (PM- ABHIM),” said an official source.

Also Read: Immunotherapy treatments are avoided by tumours by forming temporary structures: Study

A recent study’s findings offer a unique idea for how tumour cells resist elimination by the immune system.
They may also aid in the development of medicines that combine immunotherapy with the targeted suppression of certain signalling pathways in tumour cells. This research was published in the journal eLife.

“Cancer immunotherapy harnesses the body’s immune system to fight cancer. Despite its remarkable success, the majority of patients who receive immunotherapy will only see their tumours shrink in size temporarily before returning, and these relapsed tumours will likely be resistant to immunotherapy treatment,” says first author Amit Gutwillig, who was a PhD student at the Carmi Lab, Tel Aviv University, Israel, at the time the study was carried out, and is now a Senior Researcher at Nucleai, Tel Aviv.

To identify tumour relapse after immunotherapy, Carmi and the team began by comparing the genetic sequences of whole genomes in primary and relapsed tumours in the same patient. Their analysis suggested that relapsed tumours do not change dramatically following immunotherapy.

Next, the team studied this process in breast cancer and melanoma, using mouse models in which immunotherapy-resistant tumours had relapsed. They administered the mice with cells from treated tumours and allowed these cells to reach a palpable size.

The team found that the cells were equally susceptible to the same immunotherapy approach as the parent tumour, although they relapsed sooner.

To better characterise the tumour cells that survived in mice following immunotherapy, the researchers isolated and studied the live tumour cells. They found that most of the cells responded to the presence of T cells – a type of immune cell that targets foreign particles – by organising into temporary formations.

These were made up of clusters of several tumour cell nuclei, which are surrounded by a single, multilayered membrane and a meshwork of cortical actin filaments. The inner cell of the formation was dense and appeared to be compacted within another cell.

To show that this result was not due to the isolation of the melanoma cells, the team also analysed tumours with fluorescently labelled cell nuclei and membranes. They found that cell-in-cell formation was more prevalent in immunotherapy-treated tumours, particularly in sites associated with tumour cell death.

Further analysis indicated that roughly half of the tumour cells that survived immunotherapy were arranged in the cell-in-cell formation. Over time, these cells returned to a single-cell state, with similar structural features to those of the parental cell line.

The team next tested whether this phenomenon occurs in human cancers. To do this, they incubated tumour cell lines with pre-activated T cells from healthy donors. They discovered that the vast majority of breast, colon and melanoma tumour cells that survived T-cell killing were organised into the cell-in-cell structure.

A three-day observation of T cells interacting with tumour cells showed that these structures were dynamic, with individual tumour cells constantly forming and disseminating from the structure.

Finally, they examined the clinical significance of this discovery by analysing malignant samples from four stage 4 melanoma patients’ numerous organs. These individuals were having their main and metastatic lymph nodes (those that had spread from the underlying tumour) surgically removed.

The researchers discovered that cell-in-cell development was common in the T-cell zone of the draining lymph nodes but not in the main tumours in all four patients. Furthermore, in a patient with untreated recurrent melanoma, most of the cells in the main tumour were single cells, whereas cell-in-cell structures were abundant in the recurring tumours.

“This previously unknown mechanism of tumour resistance highlights a current limitation of immunotherapy,” says senior author Yaron Carmi, Principal Investigator at the Department of Pathology, Sackler School of Medicine, Tel Aviv University.

Yaron added, “Over the past decade many clinical studies have used immunotherapy followed by chemotherapy. But our findings suggest that timed inhibition of relevant signalling pathways needs to occur alongside immunotherapy to prevent the tumour from becoming resistant to subsequent treatments.”

Also Read: Delayed action hearing loss treatment triggers dementia, depression and cognitive disorders: Report

Diabetes is linked to weakened immunity and repeated illnesses. According to researchers at Sweden’s Karolinska Institutet, patients with diabetes have reduced amounts of the antimicrobial peptide psoriasin, which impairs the urinary bladder’s cell barrier, increasing the risk of urinary tract infection.

The study’s findings were reported in Nature Communications. Diabetes is caused by a shortage of insulin and/or a reduction in insulin activity. Insulin is a hormone that controls glucose (sugar) and consequently the delivery of energy to cells. Type 1 diabetes occurs when the body stops generating insulin, but type 2 diabetes occurs when the cells become less responsive to insulin, contributing to high blood glucose levels. Diabetes is a prevalent condition that has a wide range of health consequences.

One impact is that it weakens the innate immune system, making many individuals more susceptible to common diseases such urinary tract infections (UTIs) caused by E. coli bacteria. These are more prone to cause general blood poisoning, sepsis, and urinary tract infection in diabetics.

An endogenous antibiotic

Karolinska Institutet researchers have recently explored whether glucose levels in persons with diabetes (type 1, type 2, or prediabetes) are associated with psoriasin, an endogenous antibiotic that is part of the innate immune system.

The researchers examined psoriasin and other peptide levels in urine, urinary bladder cells, and blood serum samples from patients to ensure that the bladder mucosa stays intact and protects against infection. The findings were subsequently confirmed in mice and urinary bladder cells infected and uninfected.

“We found that high glucose concentrations reduce the levels of the antimicrobial peptide psoriasin, while insulin has no effect,” says Annelie Brauner, professor at the Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet who led the study. “People with diabetes have lower levels of psoriasin, which weakens the cells’ protective barrier function and increases the risk of bladder infection.”

Oestrogen therapy reduced bacterial population

Professor Brauner’s research group has previously shown that treatment with oestrogen restores the protective function of bladder cells in humans and mice and thereby help to regulate the immune response to a UTI. The researchers therefore tested how oestrogen treatment affects infected cells exposed to high glucose concentrations. They found that the treatment boosted levels of psoriasin and reduced bacterial populations, indicating that the treatment may have an effect also among patients with diabetes.

“We now plan to probe deeper into the underlying mechanisms of infections in individuals with diabetes,” says the study’s lead author Soumitra Mohanty, researcher at the same department at Karolinska Institutet. “The ultimate goal is to reduce the risk of infection in this growing patient group.”

Also Read: Adult ADHD linked to elevated risk of cardiovascular diseases, study suggested

According to a major observational research, those with ADHD are at a higher risk of acquiring a variety of cardiovascular problems than those without the disorder.

With a global incidence of roughly 2.5 percent in adults, attention deficit/hyperactivity disorder (ADHD) is one of the most frequent neurodevelopmental diseases. It is frequently co-occurring with other mental and physical disorders, some of which have been related to an increased risk of cardiovascular disease (CVD). However, whether ADHD is connected with general and particular cardiovascular illnesses has gotten less study.

The current study aimed to uncover the link between ADHD and 20 different cardiovascular illnesses when it was removed from other known risk factors such as type 2 diabetes, obesity, smoking, sleep issues, and mental disorders.

“We found that adults with ADHD were more than twice as likely to develop at least one cardiovascular disease, compared with those without ADHD,” says the study’s first author Lin Li, postdoctoral researcher at the Department of Medical Epidemiology and Biostatistics, Karolinska Institutet. “When we accounted for other well-established risk factors for CVDs, the association weakened but still remained significant, which indicates that ADHD is an independent risk factor for a wide range of cardiovascular diseases.”

The findings are based on data from a national registry of over five million Swedish citizens, including 37,000 persons with ADHD. After an average of 11.8 years of follow-up, 38 percent of people with ADHD had at least one cardiovascular disease diagnosis, compared to 24 percent of people without ADHD.

The risks for all types of cardiovascular disorders were higher, but mainly for cardiac arrest, hemorrhagic stroke, and peripheral vascular diseases. The link was somewhat greater in males than in women. Some mental comorbidities, particularly food and drug use problems, elevated the risk of cardiovascular disease in patients with ADHD considerably.

Stimulants and other psychiatric treatments, such as antidepressants and anxiety medications, had no effect on the relationship between ADHD and cardiovascular disease.

The researchers point out that because the study was observational, the data cannot demonstrate a causal association.

“Clinicians needs to carefully consider psychiatric comorbidity and lifestyle factors to help reduce the CVD risk in individuals with ADHD, but we also need more research to explore plausible biological mechanisms, such as shared genetic components for ADHD and cardiovascular disease,” says the study’s last author Henrik Larsson, professor at the School of Medical Sciences, Orebro University, and affiliated researcher at Karolinska Institutet.

Also Read: Protein restriction may be useful in reducing obesity, diabetes: Study

Reduced protein consumption, according to one study, can help manage metabolic syndrome and several of its primary symptoms, such as obesity, diabetes, and high blood pressure (hypertension).

The study’s findings were published in the journal Nutrients. Hypertension, excessive blood sugar, extra body fat around the waist, and abnormal cholesterol levels are all symptoms of metabolic syndrome, a group of disorders that increase the risk of cardiovascular disease, stroke, and diabetes.

“The study showed that cutting protein intake to 0.8 g per kg of body weight was sufficient to achieve almost the same clinical results as restricting calories, but without the need to reduce calorie intake. The results suggest that protein restriction may be one of the key factors leading to the known benefits of dietary restriction. Protein restriction dieting may therefore be a more attractive nutritional strategy and easier to follow for people with metabolic syndrome,” said Rafael Ferraz-Bannitz, first author of the article and currently a postdoctoral researcher at the Joslin Diabetes Center in Harvard Medical School in the United States.

FAPESP supported the study through a PhD scholarship provided to Ferraz-Bannitz at the University of Sao Paulo’s Ribeirao Preto Medical School (FMRP-USP) in Brazil. The study also benefited from a FAPESP Thematic Project on methodologies for simulating the effects of dietary restriction, which was supervised by Marcelo Mori, a professor at Brazil’s State University of Campinas (UNICAMP).

The study was carried out by a multidisciplinary team of scientists from the University of Copenhagen in Denmark, the University of Sao Paulo and the National Cancer Institute (INCA) in Brazil, as well as the Obesity and Comorbidities Research Center (OCRC), a Research, Innovation and Dissemination Center (RIDC) funded by FAPESP and hosted by UNICAMP.

Controlled protein diet

In the study, 21 volunteers with metabolic syndrome were analyzed for a period of 27 days during which their diet was monitored. Throughout the period, they were inpatients at FMRP-USP’s teaching hospital (Hospital das Clinicas in Ribeirao Preto).

Each volunteer’s daily calorie intake was calculated as a function of baseline metabolism (energy expenditure at rest). One group was fed what the authors call a standard Western diet (50% carbohydrate, 20% protein and 30% fat) but with 25% fewer calories.

For the second group, protein intake was reduced to 10%. Calorie intake was tailored to each volunteer’s baseline energy expenditure. Both groups consumed 4 g of salt per day.

The results showed that both the calorie and protein restriction groups lost weight owing to a decrease in body fat and that the symptoms of metabolic syndrome improved. Decreased body fat is known to be associated with reduced blood sugar and more normal levels of lipids and blood pressure.

“After 27 days of monitoring, both groups had similar results in terms of lower blood sugar, weight loss, controlled blood pressure, and lower levels of triglycerides and cholesterol. Both diets improved insulin sensitivity after treatment. Body fat decreased, as did waist and hip circumference, but without loss of muscle mass,” said Maria Cristina Foss de Freitas, last author of the article and a professor at FMRP-USP.

The findings confirmed those of previous studies involving experiments on mice. “Here, however, we succeeded in conducting a fully controlled randomized clinical trial lasting 27 days, with a personalized menu designed to meet each patient’s needs,” Foss de Freitas said.

Manipulation of dietary macronutrients – protein, carbohydrate and fat – is sufficient to obtain the beneficial effects of dietary restriction. “We demonstrated that protein restriction reduces body fat while maintaining muscle mass. That’s important since the weight loss resulting from restrictive diets is often associated with loss of muscle mass,” Ferraz-Bannitz said.

The study did not investigate the molecular mechanisms that could explain the beneficial effects of protein restriction diets, but the researchers believe low protein intake triggered a change in the metabolism or enhanced the organism’s energy management by leading it to burn fat in order to produce energy for cells. “We only have hypotheses so far. One is that molecular pathways are activated to interpret the reduction in essential amino acids as being a signal to reduce food intake while leading to the production of hormones that typically increase when we’re fasting,” Mori said. “Studies in animal models have shown the involvement of such pathways in the effects of both protein and calorie restriction, both of which lead to fat loss.”

Despite the promising results of their studies, the researchers point out that the diets involved were personalized. Mori also stressed that they focused on a specific population of patients with metabolic syndrome (obesity, diabetes, hypertension and abnormal levels of cholesterol).

“Nevertheless, it’s tempting to extrapolate the results. We know research has shown vegan diets to be positive for cases of metabolic syndrome. It’s also been found that the excessive protein intake common in the standard Western diet can be a problem. Every case should be analyzed on its own merits. We shouldn’t forget protein deficiency can lead to severe health problems, as has been well-described in pregnant women, for example,” he added.

Also Read: There is genetic relationship between capacity to move to music rhythms: Study

According to studies, there is a genetic relationship between the capacity to move to music rhythms.

69 genetic variations related with beat synchronisation, or the capacity to move in time with the beat of music, were recently discovered in the first large-scale genomic investigation of musicality.

An worldwide collaboration of experts, including the Vanderbilt Genetics Institute and 23andMe, discovered that the ability to move in time with a musical rhythm (beat synchronisation) is partially encoded in the human genome. Nature Human Behaviour reported the findings.

According to co-senior author Reyna Gordon, PhD, associate professor in the Department of Otolaryngology-Head and Neck Surgery and co-director of the Vanderbilt Music Cognition Lab, many of the genes associated with beat synchronisation are involved in central nervous system function, including genes expressed very early in brain development and in areas underlying auditory and motor skills.

“Rhythm is impacted by hundreds of genes, not simply a single gene,” Gordon explained. “Tapping, clapping, and dancing in time with the music is at the heart of our human musicality.”

The study also showed that beat synchronisation has some genetic architecture in common with other features like as walking, breathing, and circadian cycles.

“”This is fresh groundwork toward understanding the biology underpinning how musicality connects to other health qualities,” said Lea Davis, associate professor of Medicine and co-senior author.

The vast research dataset from 23andMe offered study data from over 600,000 consumers who agreed to participate in the research, allowing researchers to find genetic variants that differ in relation with persons’ capacity to beat synchronise.

“The enormous number of consenting study participants provided our group with a unique chance to catch even modest genetic signals,” said David Hinds, PhD, a research fellow and statistical geneticist at 23andMe. “These findings reflect a significant advance in our knowledge of the connections between genetics and musicality.”

Also Read: New research reveals how circadian clock aids brain recovery after damage

The study’s findings “made new connections between the genetic and neural architecture of musical rhythm, thus improving our understanding of how our genomes tune our brains to the beat of the music,” according to first author Maria Niarchou, PhD, research assistant professor in the Department of Medicine.

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A kind of brain cell that can regenerate itself is governed by circadian rhythms, according to new study from Children’s National Hospital, revealing vital insights into how the body’s internal clock may assist recovery after catastrophic brain injuries (TBI).

The findings, published in the most recent edition of eNeuro, offer up new lines of inquiry for future TBI treatments. Currently, these injuries are treated only with supportive care and rehabilitation, rather than with targeted pharmacological therapy alternatives. The findings also highlight the need of correcting circadian disruptions in order to help wounded brains repair. The circadian clock is the 24-hour rhythm that many of the body’s cells follow, which is dictated by their genes.

The Children’s National research team revealed that NG2-glia, or oligodendrocyte precursor cells, a relatively new form of brain cell, also has a circadian rhythm. This cell type is one of the few that continues to self-renew throughout adulthood and is most proliferative in the first week following a brain injury.

“We discovered evidence for the role of this well-known molecular pathway – the molecular circadian clock – in regulating the ability of these NG2-glia to proliferate, both at rest and after injury,” said Terry Dean, M.D., PhD, critical care specialist at Children’s National and the paper’s lead author. “This will serve as a starting point for further research into the processes governing cellular regeneration and optimising damage repair.”

TBI, sometimes known as “the hidden pandemic,” affects an estimated 69 million people globally each year, with injuries ranging from minor concussions to serious traumas that result in death or permanent disability. TBI affects roughly 2.8 million individuals in the United States alone each year, including 630,000 children. TBI is the largest cause of mortality in those under the age of 45, and those who survive are frequently left with long-term physical, cognitive, and psychosocial impairments.

Despite the fact that there are no specific therapeutics for TBI, there is an urgent need to discover the processes that might enable the regeneration of these NG2-glia cells, which are the most prevalent kind of brain cell known to multiply and self-renew in adult brains.

Also Read: Scientists have developed facemask that can detect virus exposure within 10 minutes

“It’s critical for researchers to understand that cell renewal is time-dependent,” said Vittorio Gallo, PhD, temporary chief academic officer and interim head of the Children’s National Research Institute. “With this information, we can go further into the body’s genetic repair process to learn more about how cells control and replenish themselves.”

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