Logopenic variant primary progressive aphasia (lvPPA) has been primarily linked to Alzheimer’s disease (AD), but newer research sheds light on the role of Lewy body disease (LBD) as well. A recent study conducted at Yonsei University Severance Hospital explored how lvPPA relates to amyloid pathology and dopaminergic degeneration, attempting to reveal more about the language and cognitive impairments faced by patients.
Among the 33 lvPPA patients studied, 20 were classified as amyloid-positive (lvPPAA+) and the remaining 13 as amyloid-negative (lvPPAA−). The researchers found notable differences between these two groups concerning their brain perfusion and dopamine transporter (DAT) uptake, both of which are indicative of various neurodegenerative processes.
“Although AD is the most common underlying pathology of lvPPA, LBD may contribute to the logopenic phenotype,” wrote the authors of the article, underscoring the potential significance of LBD beyond mere coincidence.
Each of the 33 lvPPA patients and 28 healthy controls (HC) underwent advanced imaging: MRI, 18F-florbetaben positron emission tomography (PET), and both early- and late-phase DAT PET scans. The comprehensive approach allowed the team to closely examine brain function alongside language capabilities.
Compared to healthy controls, the lvPPAA+ individuals exhibited overall lower brain perfusion across widespread areas. The lvPPAA− group also showed perfusion deficits, mainly localized to the left supramarginal and angular gyri, both areas known to be integral to language processing.
Language function evaluations indicated similar deficits across both lvPPAA+ and lvPPAA−, with both groups exhibiting substantial challenges on language tasks. It led the authors to conclude, “Lower AQ and repetition scores were associated with reduced perfusion in the left temporal and inferior parietal cortices...,” indicating strong ties between neuroimaging results and language performance.
This study marks the first time researchers have pointed to differences between language and brain health among amyloid-negative lvPPA participants, generating greater curiosity about the layered nature of this condition. The findings suggest dopaminergic depletion, typical of LBD, could be impacting language deficits more than previously recognized.
Given the high rates of dopaminergic degeneration confirmed through DAT imaging—both lvPPAA+ and lvPPAA− groups demonstrated lower DAT uptake—implications for treatment could be significant. This opens up discussions on targeted therapies for those with lvPPA presented alongside symptoms of LBD.
By enhancing our knowledge of how various neurodegenerative conditions like LBD intersect with language impairment, this study aims to lay groundwork for future studies. The authors encourage more investigations to explore this intersectionality and the multifaceted nature of lvPPA.
The blend of these findings contributes new evidence to medical literature and clinical practice, prompting both clinicians and researchers to redefine how they understand and interpret lvPPA diagnostics and treatment.
Overall, the findings bolster the idea of diversifying diagnostic and therapeutic strategies for patients with lvPPA and encourage consideration of pathology beyond just Alzheimer’s disease. The exploration of LBD's role among these patients could be important for tailoring more effective interventions and improving patient outcomes.