Aug 5, 2026
Language analysis outperforms standard tests in spotting cognitive issues
Written by Marisa Horak, MS | July 28, 2026
- Language analysis of storytelling detected Parkinson's cognitive issues better than standard tests.
- Parkinson's patients showed reduced storytelling accuracy, organization, and sometimes verbosity.
- This method offers a nuanced look at episodic memory problems in Parkinson's.
Language-based analyses of how people with Parkinson’s disease tell stories may provide a more nuanced look at how the disease affects memory and cognition, according to a study.
In fact, the data suggest that a language-based approach can distinguish between people with or without Parkinson’s more accurately than standard cognitive tests. The researchers called for further studies on how this type of language analysis might be deployed to monitor cognitive changes in patients with Parkinson’s.
An early-access version of the study, “Digitizing episodic memory assessments in Parkinson’s disease via natural language processing,” was published in npj Parkinson’s Disease.
Parkinson’s is a neurological disorder that often causes memory and cognition problems. One of the more common manifestations of Parkinson’s-related cognitive challenges is problems with episodic memory — that is, the ability to recall and recount specific events, such as a trip or a party.
A range of standardized cognitive tests is routinely used to check for memory issues in Parkinson’s. Most of these tests assess how well a person can recall facts — for example, by providing a list of numbers and later asking the person to recite it.
Taking a nuanced approach
But memory isn’t just about recalling discrete facts. This is especially true for episodic memory: A person’s memory of an event includes not only what happened, but also their emotions and sensory experiences. Standard cognitive tests that assess only how well people recall facts may miss key nuances in how memory is affected in people with Parkinson’s.
An international team of scientists tested a different approach, using a computer-based analytical technique called natural language processing. They had patients read two stories — one action-based, focused on movement, and one more focused on internal emotions — and then recount both. A computer then analyzed the patients’ words.
The computer looks at three factors: verbosity, or how many different types of words the person uses; semantic acuity, which refers to how accurately the facts of the story are recalled; and organizational similarity, which evaluates whether the patient’s retelling matches the structure of the original story.
To test this approach, the researchers recruited 35 people with Parkinson’s and 39 control participants without the disease. They found that, for both types of stories, those with Parkinson’s showed reduced semantic acuity and lower organizational similarity compared with controls. Parkinson’s patients were also less verbose than controls on the action story, though verbosity was similar for the emotion-focused story.
Aug 4, 2026
Hybridopa program leads to changes in brain networks involved in movement
Written by Michela Luciano, PhD | July 28, 2026
- Hybridopa, a digital app combined with levodopa, eased Parkinson's motor symptoms.
- This therapy induced structural and functional brain changes, suggesting neuroplasticity.
- It offers an integrated treatment approach for Parkinson's, with a Phase 3 trial planned.
Patients participating in a three-week digital intervention program designed to complement levodopa, the standard treatment for Parkinson’s disease, showed measurable structural and functional changes in brain networks involved in movement, accompanied by meaningful easing of motor symptoms.
The pilot study evaluated Remepy‘s investigational hybrid therapy, Hybridopa, in 32 adults with Parkinson’s disease who had participated in a Phase 2a trial. That study showed that people receiving Hybridopa, which combines levodopa with a prescription digital program called DopApp, experienced greater easing of motor and nonmotor symptoms than those given levodopa along with a placebo app.
The Phase 2a trial also found functional changes in brain networks involved in movement and mood regulation. The new findings add evidence of structural changes in those movement-related brain networks.
Remepy said the results suggest that Hybridopa may promote neuroplasticity — the brain’s ability to reorganize and strengthen its neural connections in response to learning — helping explain the clinical benefits seen in the earlier trial.
“Our Phase IIa trial showed that Hybridopa delivers meaningful clinical improvements for people living with Parkinson’s disease,” Or Shoval, cofounder and co-CEO of Remepy, said in a company press release. “This publication helps explain the neural mechanisms underlying those effects.”
Phase 3 trial planned
“Together, these findings support a shift in Parkinson’s treatment toward integrated approaches that combine pharmacological therapy with structured, system-level digital interventions,” said Michal Tsur, PhD, cofounder and co-CEO of Remepy. “This growing body of clinical and mechanistic evidence … is what motivates us to advance Hybridopa into Phase III later this year.”
The study, “Local and global microstructural and functional thalamomotor connectivity alterations in Parkinson’s disease following motor learning,” was published in npj Parkinson’s Disease.
Parkinson’s is caused by the progressive loss of nerve cells that produce dopamine, a brain chemical essential for controlling movement. In addition to motor symptoms, the disease can also cause nonmotor problems, including cognitive impairment. Although levodopa remains the standard Parkinson’s treatment, some motor symptoms often remain inadequately controlled.
Aug 3, 2026
Study found no clear p-tau217 link in patients without dementia
Written by Michela Luciano, PhD | July 29, 2026
- The Alzheimer’s marker p-tau217 was not clearly linked to early cognitive problems in people with Parkinson’s who did not have dementia.
- Early cognitive impairment in Parkinson’s may primarily result from Parkinson’s-related mechanisms.
- Further brain imaging studies are needed to validate the findings and clarify the role of Alzheimer’s-related pathology.
Alzheimer’s-related brain changes may not be a major contributor to earlier cognitive problems in people with Parkinson’s disease who have not developed dementia, a new study suggests.
Researchers found that blood levels of phosphorylated tau-217 (p-tau217), a blood marker of early Alzheimer’s disease, were not clearly associated with cognitive impairment. The findings suggest that early cognitive changes in Parkinson’s may primarily result from the disease itself, with coexisting Alzheimer’s-related changes potentially playing a larger role in people who develop dementia, the researchers noted.
The researchers cautioned, however, that p-tau217 may have limited sensitivity for detecting Alzheimer’s-related pathology in people with Parkinson’s. Further studies using brain imaging are needed to validate the findings.
Study examines Alzheimer’s marker in early cognitive problems
The study, “Association Between Plasma Phosphorylated Tau-217 and Cognition in Parkinson’s Disease,” was published in Movement Disorders.
Cognitive impairment affects about one in 10 people in the early stages of Parkinson’s, and becomes more common as the disease progresses, affecting up to three-quarters of people in later stages. Its timing and severity vary considerably from person to person.
Studies examining brain tissue of people with Parkinson’s after their death have found Alzheimer’s-related changes, including accumulations of amyloid-beta protein and neurofibrillary tangles of tau protein, in up to 40% of those who developed Parkinson’s-related dementia. Brain imaging studies have also linked these changes to poorer cognitive function.
However, most of this research has “focused on Parkinson’s-related dementia, the later stage of [Parkinson’s]-associated cognitive impairment, leaving open questions about the degree to which [Alzheimer’s-related disease] contributes to earlier/milder cognitive impairment in [Parkinson’s],” the researchers wrote.
To help answer that question, researchers in Canada examined whether blood p-tau217 levels were associated with earlier cognitive impairment in people with Parkinson’s who had not developed dementia.
The team analyzed blood p-tau217 measurements from 165 people with Parkinson’s who did not have dementia and 58 healthy controls enrolled through the Quebec Parkinson Network, a registry of people with Parkinson’s and healthy volunteers.
The analysis included participants who had completed a comprehensive battery of neuropsychological tests or the Montreal Cognitive Assessment (MoCA), a commonly used screening test for cognitive impairment. The neuropsychological tests evaluated attention and working memory, executive function, memory, language, and visuospatial abilities. Information on self-reported cognitive difficulties was available for 157 participants with Parkinson’s.
Jul 31, 2026
Specific ceramide ratio and inflammation combine to signal risk
Written by Michela Luciano, PhD | July 30, 2026
- A specific blood ceramide ratio is linked to worsening cognitive decline in Parkinson's disease.
- Higher levels of this ratio predict poorer cognitive performance, partially mediated by inflammation.
- This blood marker could help identify Parkinson's patients at risk for thinking and memory problems.
Higher blood levels of a specific ratio between two fats, called ceramides, may help identify people with Parkinson’s disease who are more likely to develop thinking and memory problems, according to a new study.
A higher Cer 24:1/Cer 24:0 ratio was closely associated with worsening cognitive impairment and remained a strong independent predictor of poorer cognitive performance after accounting for other factors. Inflammation appeared to partially mediate this association, highlighting ceramide metabolism and inflammatory signaling as complementary biological features of cognitive impairment in Parkinson’s disease.
“These findings establish a ceramide-centered quantitative framework integrating metabolic and inflammatory dimensions of cognitive impairment in [Parkinson’s], supporting stratified biomarker development,” researchers wrote.
The study, “Plasma ceramide ratios define metabolic–inflammatory associations with cognitive impairment in Parkinson’s disease,” was published in npj Parkinson’s Disease.
Cognitive changes often detected after damage has occurred in brain
A progressive neurological disorder, Parkinson’s is most known for causing motor symptoms, but it can also affect thinking and memory. Cognitive impairment can range from mild difficulties with attention, planning, and language to dementia, which develops in up to 80% of people with Parkinson’s over the course of the disease.
These cognitive changes are often detected only after significant damage has already occurred in the brain, limiting opportunities for early intervention. This “diagnostic lag,” together with the wide variation in the progression of cognitive impairment from person to person, highlights the need for accessible biomarkers that reflect the biological processes underlying cognitive decline, according to researchers.
One group of promising candidates is ceramides, a family of fatty molecules that help maintain nerve cell membranes, regulate communication between nerve cells, and modulate inflammation. Previous studies have linked abnormal ceramide metabolism to Parkinson’s and faster cognitive decline.
However, the specific ceramide profiles associated with different stages of cognitive impairment remain unclear, as do their relationships with inflammation and biomarkers of neurodegeneration.
To address this gap, researchers in China analyzed blood samples from 408 people with Parkinson’s, 98 people with multiple system atrophy (MSA), a neurological disorder that shares many symptoms with Parkinson’s, and 220 healthy adults.
Jul 30, 2026
1 therapy, bevemipretide, was shown to ease brain inflammation in mice
Written by Andrea Lobo | July 16, 2026
- Massachusetts-based biotech Mighty Therapeutics has raised $150 million to advance treatments for Parkinson's and other diseases.
- One drug in its pipeline is bevemipretide, which was shown to reduce brain inflammation in mice.
- The company's work targets the dysfunction of mitochondria, which are energy-producing structures in cells.
Mighty Therapeutics, a Massachusetts-based biotech company, announced that it has raised $150 million to support the clinical development of its treatment candidates for Parkinson’s disease and other neurodegenerative conditions.
The new funding is expected to expedite pipeline initiatives in Parkinson’s as well as ongoing late-stage drug development programs in other diseases, according to a company press release detailing the financing.
The biotech’s work focuses on mitochondria, small energy-producing structures inside cells that serve as their powerhouses, whose dysfunction has been linked to a number of conditions marked by nerve cell loss, including Parkinson’s and amyotrophic lateral sclerosis (ALS).
In Mighty’s pipeline is bevemipretide (SBT-272), a small molecule designed to improve mitochondrial function. In a mouse model of Parkinson’s, the treatment candidate was found to reduce markers of brain inflammation.
The developer says it will use the new funding to “progress commercial and clinical development of [a] new class of mitochondrial targeted medicines.”
“These financings … [support] our continued leadership of the burgeoning field of mitochondrial medicine across a broad range of therapeutic areas,” said Reenie McCarthy, Mighty’s CEO. “With our strong commercial momentum and promising pipeline, we are poised for long-term growth and continued patient impact.”
Parkinson’s is caused by the progressive loss of dopaminergic neurons, which are nerve cells that produce dopamine, a signaling molecule that plays a role in voluntary movement. Several mechanisms are thought to contribute to neuronal damage and loss in Parkinson’s, including the accumulation of toxic clumps, or aggregates, of misfolded alpha-synuclein protein and mitochondrial dysfunction.
Misfolded alpha-synuclein can bind to cardiolipin, a fatty molecule found in the inner membrane of mitochondria, reducing their ability to produce energy.
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