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Category: neuroscience – Page 18

Research highlights solutions to critical gaps in dementia and childhood cancer care

In the United States, significant numbers of adults with dementia require long-term care services. For example, around 750,000 people who live in nursing homes have a diagnosis of dementia. However, transportation insecurity for this population has not received sufficient attention. Although long-term care facilities provide basic medical services, residents with dementia often need external, preventative, and follow-up care such as specialist visits, diagnostics, and dental or vision services. Without reliable nonemergency medical transportation, these needs may go unmet.

To demonstrate the extent of this problem, Postdoctoral Research Scientist Soojeong Han, Ph.D., and her colleagues reviewed existing literature on non-emergency medical for individuals with living in long-term care (LTC) facilities. The study, “Transportation Services in Society for Individuals Living With Dementia in Long-Term Care Facilities: A Scoping Review,” was published in the Journal of the American Medical Directors Association.

Their review found only five publications that mentioned this topic, and even then, only briefly. Across these studies, caregivers, health care professionals, and people with dementia consistently described nonemergency medical transportation as a critical need. Reported barriers included financial strain, rural-urban disparities, lack of continuity among transportation vendors, and dementia-specific challenges such as , stigma, and the need for caregiver accompaniment.

Scientists just found a molecule that could stop Parkinson’s in its tracks

Researchers have designed a peptide that prevents the deadly misfolding of alpha-synuclein, the protein behind Parkinson’s and some dementias. In lab and animal tests, it stabilized the protein and improved motor function. The work demonstrates the power of rational drug design in tackling brain diseases that have long lacked effective treatments.

1 Gene, 1 Disease no More — Acknowledging The Full Complexity of Genetics Could Improve And Personalize Medicine

Your DNA contains millions of genetic variants that interact with each other in ways that affect whether diseases such as schizophrenia and heart disease develop, and with what severity.

Rethinking Alzheimer’s: Why this common gene variant is bad for your brain

The suspected causes of Alzheimer’s disease are diverse, and its cures are, today, nonexistent.

What’s all but certain is that many who today have the mental chops to wade through a detailed article about the disorder’s drivers and demographics will nevertheless succumb to it someday.

With no cure available, despite numerous attempts to find one, researchers are looking down new roads for treatments. A recent discovery by Stanford Medicine neurologist Mike Greicius, MD, may help clear one of those roads for faster passage.

Scientists fix genetic defect in mice tied to brain disorders that include autism and epilepsy

In an exciting scientific first, researchers at the Allen Institute successfully designed a new gene therapy that reversed symptoms related to SYNGAP1-related disorders (SRD) in mice. These are a class of brain disorders that can lead to severe and debilitating symptoms including intellectual disability, epilepsy, motor problems, and risk-taking behaviors in humans. In most cases, SRDs are caused when someone has only one working copy of the SYNGAP1 gene instead of the normal two.

The findings, recently published in the journal Molecular Therapy, represent the first successful gene supplementation therapy for SRDs in which an adeno associate virus (AAV) was used to deliver a working copy of the SYNGAP1 gene into . AAVs are non-replicating viruses that act like delivery trucks carrying therapeutic cargo, in this case the SYNGAP1 gene, into cells that need it.

“Gene supplementation is providing a functional new copy of a defective gene, a strategy that has great potential for correcting diseases where a gene is completely missing or where a single copy of a gene is lost,” said Boaz Levi, Ph.D., associate investigator at the Allen Institute and senior author of the study. “This provides a clear demonstration that SYNGAP1-related disorders can be treated with a neuron-specific gene supplementation strategy. It’s an important milestone for the field that provides hope for those who suffer from this class of severe neurological diseases.”

Synaptic Dysfunction in Dementia Can Be Modelled in Patient-Derived Neurons

Neurons produced from frontotemporal dementia patients’ skin biopsies using modern stem cell technology recapitulate the synaptic loss and dysfunction detected in the patients’ brains, a new study from the University of Eastern Finland shows.

Frontotemporal dementia is a progressive neurodegenerative disease affecting the frontal and temporal lobes of the brain. The most common symptoms are behavioral changes, difficulties in understanding or producing speech, problems in movement, and psychiatric symptoms. Often, frontotemporal dementia has no identified genetic cause, but especially in Finnish patients, hexanucleotide repeat expansion in the C9orf72 gene is a common genetic cause, present in about half of the familial cases and in 20 per cent of the sporadic cases where there is no family history of the disease. However, the disease mechanisms of the different forms of frontotemporal dementia are still poorly understood, and there are currently no effective diagnostic tests or treatments affecting the progression of the disease in clinical use.

Brain imaging and neurophysiological studies have shown that pathological and functional changes underlying the symptoms occur at synapses, the connections between brain neurons, in frontotemporal dementia patients. PET imaging studies have shown significant synapse loss in the brain, and transcranial magnetic stimulation, on the other hand, has indicated disturbed function of both excitatory and inhibitory neurotransmitter systems, leading to deficient neurotransmission. Often, drugs affecting the different neurotransmitter systems are used to mitigate the symptoms of frontotemporal dementia patients.

Chinese medicine extract tetrandrine’s precise mechanism of action opens new avenues for drug discovery

With this discovery, the researchers propose that tetrandrine can be used to disrupt processes critical to the survival and replication of viruses, such as Ebola and COVID-19, by targeting LIMP-2 to alter lysosomal calcium release.

Importantly, these findings highlight lysosome-related mechanisms as a new frontier for , offering novel strategies for treating diseases caused by calcium imbalance, including neurodegenerative disorders like Alzheimer’s and Parkinson’s, as well as certain metastatic cancers.

Prof. Ko said, “This is the first time a function of LIMP-2 in calcium signaling has been uncovered. From a cell biology perspective, our study has revealed a completely new pathway for NAADP-regulated calcium signaling, through LIMP-2 and sphingosine. From an anti-viral treatment perspective, the study has identified LIMP-2 as a key target of tetrandrine for the treatment of Ebola virus infection, with broader applications in other antiviral therapies.”

Children of parents with mental disorders may face higher risk of early death

Research led by the Karolinska Institutet reports that offspring of parents with mental disorders face increased mortality, with the highest risks for unnatural deaths and when both parents had diagnoses.

Parental mental disorders have been linked to and to multiple developmental, mental, and somatic outcomes, while links with long-term offspring mortality remained unclear.

In the study, “Parental Mental Disorders and Offspring Mortality up to Middle Age,” published in JAMA Psychiatry, researchers conducted a nationwide register-based cohort study to investigate associations between parental mental disorders and mortality in offspring up to .

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