Category Archives: Research News (General)

Directly involving the thousands of family members and friends who serve as ‘informal carers’ for people with dementia in the evaluation of patients’ symptoms and behaviour could offer improved insights for healthcare professionals and help alleviate feelings of stress, guilt and isolation felt by many who fulfil these duties, a new study published in Dementia has found.

The findings highlight a need for more structured educational programmes covering broader knowledge around the disease for informal carers, who often have no formal training or support networks to depend on. Information on disease progression, guidelines on dealing with challenging behaviours and financial and legal advice could better prepare carers about what to expect.

The research, conducted by an inter-disciplinary team of experts, collated insights from carers and health care professionals and identified key themes which capture the main challenges faced by carers, as well as the type of support they want from health care services.

Previous research found that informal caregivers of people with dementia often display increased levels of depression and stress as well as poor self-rated health.

The new findings show that existing health and social care services are often fragmented which can make communication between healthcare professionals and care providers difficult. Healthcare professionals also stated that while they have a theoretical knowledge of the disease, they felt they often lack knowledge of how it is to live with dementia which can make it difficult to know how best to support caregivers.

The researchers say they hope that the findings will lead to improvements in dementia care with a goal of creating a better educational package for carers.

Paper: “Caregivers’ interactions with health care services – Mediator of stress or added strain? Experiences and perceptions of informal caregivers of people with dementia – A qualitative study”
Reprinted from materials provided by the University of Lincoln.

Increasing the amount of social interaction for people with dementia living in care homes to just one hour a week improves quality of life when combined with personalised care, according to a new study.

A large-scale trial  found that the approach also saves money.

Previous research has found that in many care homes, residents have as little as two minutes of social interaction per day.

The new research, published in PLOS Medicine, upskilled key care home staff to deliver person-centred care. That involves simple measures such as talking to residents about their interests and involving them in decisions around their own care.

When combined with just one hour a week of social interaction, the programme improved quality of life and reduced agitation and aggression in people with dementia.

The trial involved more than 800 people with dementia across 69 care. Two ‘care staff champions’ at each home were trained over four day-long sessions to take simple measures that such as involve talking to residents about their interests and decisions around their own care. Importantly, the approach also saved money compared to standard care.  Researchers say the next key challenge is to roll the programme out across care homes to benefit the lives of people with dementia living in these facilities.

Paper: “Impact of person-centred care training and person-centred activities on quality of life, agitation, and antipsychotic use in people with dementia living in nursing homes: A cluster-randomised controlled trial”
Reprinted from materials provided by University of Exeter.

After more than a decade of research, this much we know: it’s good for your brain to know another language.

A new study, published in Neuropsychologia,  goes further, however, focusing specifically on the effects of knowing a second language for patients with Alzheimer’s disease (AD) and mild cognitive impairment (MCI).

Unlike previous studies using CT scans, the researchers  used high-resolution, whole-brain MRI data and sophisticated analysis techniques to investigate language and cognition control areas in the frontal regions of the brain, and medial temporal lobe structures that are important for memory and are brain areas known to atrophy in MCI and AD patients.

Their sample included 34 monolingual MCI patients, 34 multilingual MCI patients, 13 monolingual AD patients and 13 multilingual AD patients.

The researchers say that their findings suggest that multilingualism is associated with increased brain plasticity and cognitive reserve. Moreover, their study indicates, they say, that people who speak more than one language may in some circumstances compensate for AD-related tissue loss by accessing alternative networks or other brain regions for memory processing, a hypothesis they hope to test in future studies.

Paper: “Structural brain differences between monolingual and multilingual patients with mild cognitive impairment and Alzheimer disease: Evidence for cognitive reserve”
Reprinted from materials provided by Concordia University.

Scientists developing a rapid, practical test for the early diagnosis of prion diseases have modified the assay to offer the possibility of improving early diagnosis of Parkinson’s disease and dementia with Lewy bodies.

The findings were published in Acta Neuropathologica Communications.

The group tested 60 cerebral spinal fluid samples, including 12 from people with Parkinson’s disease, 17 from people with dementia with Lewy bodies, and 31 controls, including 16 of whom had Alzheimer’s disease. The test correctly excluded all the 31 controls and diagnosed both Parkinson’s disease and dementia with Lewy bodies with 93 percent accuracy.

Importantly, test results were available within two days, compared to related assays that require up to 13 days. The group conducted the tests using Real-Time Quaking-Induced Conversion (RT-QuIC), an assay developed and refined over the past decade.

Multiple neurological disorders, including Parkinson’s disease and dementia with Lewy bodies, involve the abnormal clumping of a protein called alpha-synuclein into brain deposits called Lewy bodies. The pathological processes in these diseases resemble prion diseases in mammal brains. Like prion diseases, Parkinson’s disease and dementia with Lewy bodies result in progressive deterioration of brain functions.

The researchers continue to adapt the RT-QuIC assay to detect additional types of neurological diseases with greater accuracy using the least invasive patient sample possible—whether that is blood, skin, nasal brushings, or other samples. The group also has trained many international colleagues to use and advance the test.

Article: “Rapid and ultra-sensitive quantitation of disease-associated α-synuclein seeds in brain and cerebrospinal fluid by αSyn RT-QuIC” 
Reprinted from materials provided by NIH/National Institute of Allergy and Infectious Diseases.

Low muscle strength during the later teen years has been identified as a risk factor for much later onset of the neurological disease known as ALS, or amyotrophic lateral sclerosis.

A study published in the Journal of Neurology also links low blood counts at a young age to ALS.

The researchers studied Swedish military enlistment data for more than 1.8 million (1,819,817) men in the 1968-2005 period as well as data from the Swedish health care register and mortality register. The majority were 18 years old at the time of enlistment. The follow-up time was up to 46 years.

The group included 526 individuals who developed ALS, a disease that usually occurs after age 50 and involves a successive degradation of the nerves that control muscles. There is no cure, and in most cases patients die after two to five years.

The current study confirms the impression that ALS can be associated with a relatively low body mass index (BMI), even at a young age. The differences, however, were not dramatic. Those who developed ALS had an average BMI of 21.1, compared with 21.9 for the group as a whole.

What stood out instead was the finding that ALS could be associated with low blood counts at military enlistment – in other words, a low proportion of oxygen-carrying red blood cells in the blood. A link was also found between ALS and measured muscle strength in the hands, arms and legs at the time of enlistment.

Paper: “Risk factors in Swedish young men for amyotrophic lateral sclerosis in adulthood”
Reprinted from materials provided by the University of Gothenburg.

With the aid of a PET camera, researchers have developed a new method for investigating the dopamine system in the brains of patients suffering from Parkinson’s disease. The method measures levels of a protein called dopamine transporter and could lead to improved diagnosis of Parkinson’s disease. The study was published in Movement Disorders.

Dopamine is a substance produced in the brain and is responsible for controlling our movements. In Parkinson’s disease, dopamine cells degenerate and their loss is responsible for the motor symptoms that characterise the disorder, such as shaking, slowness of movement and difficulty walking.

Using Positron Emission Tomography (PET), a group of researchers have measured the levels of the dopamine transporter protein DAT that regulates the levels of dopamine in the brain. DAT functions as a biomarker for dopamine cells and is present on the surface of the dopamine cells in the cell bodies, on the nerve fibres and on the nerve endings. By measuring where DAT is found, researchers have been able to map the presence of dopamine cells.

The study was based on 20 patients suffering from mild Parkinsonism and an equal number of healthy individuals. The results showed significantly lower amounts of DAT in nerve endings in the Parkinson’s patients than those not suffering from the disease.

Future studies will examine patients with more advanced Parkinson’s, in order to gain a greater understanding of the links between DAT and clinical variables such as motor symptoms and the various stages of the disease.

Paper: “Nigrostriatal dopamine transporter availability in early Parkinson’s disease”
Reprinted from materials provided by Karolinska Institutet.

A team of researchers has found that gradually depleting an enzyme called BACE1 reverses the formation of amyloid plaques in the brains of mice with Alzheimer’s disease, thereby improving the animals’ cognitive function. The study was published in the Journal of Experimental Medicine.

An early event in Alzheimer’s is the abnormal buildup of beta-amyloid peptide, which can form large amyloid plaques in the brain and disrupt the function of neuronal synapses. BACE1 helps produce beta-amyloid peptide by cleaving amyloid precursor protein (APP).

Researchers have hypothesized that inhibiting BACE1 could keep the plaques from appearing. However, BACE1 controls many important processes by cleaving proteins other than APP, and mice completely lacking BACE1 have been shown to suffer severe neurodevelopmental defects.  For this study, the researchers  generated mice that gradually lose this enzyme as they grow older. These mice were shown to develop normally and appeared to remain perfectly healthy over time.

The researchers then bred these rodents with Alzheimer’s mice. The resulting offspring also formed plaques at this age, even though their BACE1 levels were approximately 50% lower than normal. Remarkably, however, the plaques began to disappear as the mice continued to age and lose BACE1 activity, until, at 10 months old, the mice had no plaques in their brains at all.

Decreasing BACE1 activity also resulted in lower beta-amyloid peptide levels and reversed other hallmarks of Alzheimer’s disease, such as the activation of microglial cells and the formation of abnormal neuronal processes.

Loss of BACE1 also improved the learning and memory of mice with Alzheimer’s disease. However, when the researchers made electrophysiological recordings of neurons from these animals, they found that depletion of BACE1 only partially restored synaptic function, suggesting that BACE1 may be required for optimal synaptic activity and cognition.

Article: “BACE1 deletion in the adult mouse reverses preformed amyloid deposition and improves cognitive functions”
Reprinted from materials provided by Rockefeller University.

Scientists have developed a novel approach for deep brain stimulation. The new method, published in Science, utilises upconversion nanoparticles to allow delivery of visible light deep into the brain to stimulate neural activities in a less-invasive manner. This innovation marks a significant breakthrough in optogenetics, empowering researchers to uncover valuable insights about the brain.

Optogenetics is a widely adopted research technique in the field of neuroscience that makes use of visible light to activate or inhibit neurons in the brain, enabling researchers to examine the brain’s functions in a minimally invasive manner. The inability of visible light to penetrate into deep brain structures, however, remains a major experimental challenge for this technique, and current deep brain stimulation still requires the insertion of an optical fibre directly into the brain.

To make deep brain stimulation less invasive, the researchers began exploring with near-infrared light, known to possess significantly higher tissue penetration capability and also relatively safe for biological samples. Using a two-step process, upconversion nanoparticles are first introduced into the brain by transcranial injection. Upon reaching deep brain, the implanted upconversion nanoparticles, a unique group of luminescent nanomaterials capable of converting near-infrared light into visible light, then generates visible light which acts to stimulate the neurons. The strategy has shown to be effective in triggering memory recall and dopamine release in the team’s experiments.

This novel approach offers a simpler, less-invasive alternative to fibre-optic implantation for deep brain stimulation, the researchers say, and holds immense potential in facilitating advancement in neuroscience.

Paper: “Near-infrared deep brain stimulation via upconversion nanoparticle–mediated optogenetics”

Reprinted from materials provided by the National University of Singapore.

Higher levels of lifestyle physical activity — such as housecleaning, walking a dog and gardening, as well as exercise — are associated with more gray matter in the brains of older adults, according to a study published in The Journal of Gerontology: Psychological Sciences.

The gray matter in the brain includes regions responsible for controlling muscle movement, experiencing the senses, thinking and feeling, memory and speech and more. The amount of gray matter in the brain often begins to decrease in late adulthood, even before symptoms of cognitive dysfunction appear.

The study measured the levels of physical activity by 262 older adults. Participants wore a noninvasive device called an accelerometer continuously for seven to 10 days. The goal was to accurately measure the frequency, duration and intensity of a participant’s activities over that time.

The use of accelerometers was only one of the ways in which this analysis differed from some other investigations of the health of older people. Most research that explores the effects of exercise relies on questionnaires, which ask participants to “self-report” their levels of activity, the researchers said. Moreover, questionnaires tend to ask in a fairly non-specific fashion about types and intensity of exercise.

The study compared gray matter volumes as seen in participants’ MRIs with readings from the accelerometers and other data, which all were obtained during the same year. The analysis found the association between participants’ actual physical activity and gray matter volumes remained after further controlling for age, gender, education levels, body mass index and symptoms of depression, all of which are associated with lower levels of gray matter in the brain.

Article: “Accelerometer Physical Activity is Associated with Greater Gray Matter Volumes in Older Adults without Dementia or Mild Cognitive Impairment”
Reprinted from materials provided by Rush University Medical Center.

Scientists have transformed skin cells from patients with Huntington’s disease into the type of brain cell affected by the disorder, creating a new tool to study the degenerative and eventually fatal neurological condition.

The study, published in Nature Neuroscience, showed that the patients’ nerve cells — converted directly from patients’ skin cells — exhibited “symptoms” of the disorder, including DNA damage, dysfunctional mitochondria and cell death. Correcting for malfunctioning genes in these reprogrammed neurons prevented the cell death that is characteristic of Huntington’s disease, an inherited genetic disorder that causes cognitive decline and involuntary muscle movements.

Huntington’s disease and other inherited brain conditions are challenging to study because it is difficult to obtain samples of neurons from living patients. Seeking the next best thing, scientists have found ways to transform skin cells into brain cells.

Their method allows skin cells to bypass the stem cell stage as they are being reprogrammed into neurons. Passing through a stem cell stage resets the developmental clock to an embryonic-like state, wiping out the age-associated effects of the disorder. But the directly reprogrammed neurons retain their age, along with the problems associated with adult-onset Huntington’s disease, according to the researchers.

The researchers say that their technique, which allows them to capture characteristics of the disease at distinct moments in its progression, may also be applied to other conditions as well.

Paper: “Striatal neurons directly converted from Huntington’s disease patient fibroblasts recapitulate age-associated disease phenotypes”
Reprinted from materials provided by Washington University School of Medicine.