Characterization of the logopenic variant of Primary Progressive Aphasia: A systematic review and meta-analysis

Conca, Francesca; Esposito, V.; Giusto, Giada; Cappa, Stefano F.; Catricalà, Eleonora

doi:10.1016/j.arr.2022.101760

Cited by 20 publications

(15 citation statements)

References 111 publications

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“…Compared to the other atypical variants of AD, the neuroimaging pattern of lvPPA is relatively homogeneous across patients and localized in the left temporoparietal, inferior parietal and posterior temporal regions [2,6]. This pattern was confirmed in a systematic review by Conca and colleagues, including 207 papers and reviewing grey matter atrophy, white matter fibre tracts, glucose metabolism and perfusion data in addition to clinical features [7 ▪▪ ]. This variant can be distinguished from other AD variants based on a higher degree of atrophy in left temporal regions (vs. tAD and PCA), a lower degree of hippocampal and entorhinal cortex atrophy (vs. tAD) and of right hippocampal and temporal regions (vs. PCA) [8].…”

Section: Logopenic Variant Of Primary Progressive Aphasiamentioning

confidence: 76%

Atypical forms of Alzheimer's disease: patients not to forget

Montembeault

Migliaccio

2023

Current Opinion in Neurology

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Purpose of review The aim of this paper is to summarize the latest work on neuroimaging in atypical Alzheimer's disease (AD) patients and to emphasize innovative aspects in the clinic and research. The paper will mostly cover language (logopenic variant of primary progressive aphasia; lvPPA), visual (posterior cortical atrophy; PCA), behavioral (bvAD) and dysexecutive (dAD) variants of AD. Recent findings MRI and PET can detect and differentiate typical and atypical AD variants, and novel imaging markers like brain iron deposition, white matter hyperintensities (WMH), cortical mean diffusivity, and brain total creatine can also contribute. Together, these approaches have helped to characterize variant-specific distinct imaging profiles. Even within each variant, various subtypes that capture the heterogeneity of cases have been revealed. Finally, in-vivo pathology markers have led to significant advances in the atypical AD neuroimaging field. Summary Overall, the recent neuroimaging literature on atypical AD variants contribute to increase knowledge of these lesser-known AD variants and are key to generate atypical variant-specific clinical trial endpoints, which are required for inclusion of these patients in clinical trials assessing treatments. In return, studying these patients can inform the neurobiology of various cognitive functions, such as language, executive, memory, and visuospatial abilities.

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Section: Logopenic Variant Of Primary Progressive Aphasiamentioning

confidence: 76%

Atypical forms of Alzheimer's disease: patients not to forget

Montembeault

Migliaccio

2023

Current Opinion in Neurology

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“…Neuroimaging shows a characteristic (left hemisphere greater than right) anterior temporal pattern of atrophy (Hodges et al, 1992;Rosen et al, 2002). The logopenic variant (lvPPA) is characterized by impaired word retrieval and phrase/sentence repetition, as well as three of the following associated features: phonological errors (i.e., well-articulated sound errors) in speech production, spared grammar, spared single word comprehension, and spared motor speech abilities (Conca et al, 2022;Gorno-Tempini et al, 2011;Rohrer et al, 2010a, b). Atrophic changes are predominantly observed in left temporoparietal areas (Gorno-Tempini & Brambati, 2008;Teichmann et al, 2013).…”

Section: Current Diagnostic Framework For Ppa and Ppaosmentioning

confidence: 99%

Behavioral Treatment for Speech and Language in Primary Progressive Aphasia and Primary Progressive Apraxia of Speech: A Systematic Review

Wauters,

Croot,

Dial

et al. 2023

Neuropsychol Rev

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Primary progressive aphasia (PPA) and primary progressive apraxia of speech (PPAOS) are neurodegenerative syndromes characterized by progressive decline in language or speech. There is a growing number of studies investigating speech-language interventions for PPA/PPAOS. An updated systematic evaluation of the treatment evidence is warranted to inform best clinical practice and guide future treatment research. We systematically reviewed the evidence for behavioral treatment for speech and language in this population. Reviewed articles were published in peer-reviewed journals through 31 May 2021. We evaluated level of evidence, reporting quality, and risk of bias using a modified version of the American Speech-Language Hearing Association (ASHA) Levels of Evidence, an appraisal point system, additional reporting quality and internal/external validity items, and, as appropriate, the Single Case Experimental DesignScale or the Physiotherapy Evidence Database – PsycBITERating Scale for Randomized and Non-Randomized Controlled Trials. Results were synthesized using quantitative summaries and narrative review. A total of 103 studies reported treatment outcomes for 626 individuals with PPA; no studies used the diagnostic label PPAOS. Most studies evaluated interventions for word retrieval. The highest-quality evidence was provided by 45 experimental and quasi-experimental studies (16 controlled group studies, 29 single-subject designs). All (k = 45/45) reported improvement on a primary outcome measure; most reported generalization (k = 34/43), maintenance (k = 34/39), or social validity (k = 17/19) of treatment for at least one participant. The available evidence supports speech-language intervention for persons with PPA; however, treatment for PPAOS awaits systematic investigation. Implications and limitations of the evidence and the review are discussed.

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“…In amnestic AD, we hypothesized that patients would have degeneration of WM projections from limbic and default-mode network regions, particularly the parahippocampal cingulum ( Pichet Binette et al, 2021 ; Raghavan et al, 2022 ). In lvPPA, we predicted patients would have left-lateralized WM degeneration affecting projections from posterior temporal and inferior parietal cortex, an established epicenter of disease in this form of aphasia ( Conca et al, 2022 ; Mandelli et al, 2023 ). In contrast, we predicted that PCA patients would exhibit a posterior-to-anterior gradient of bilateral WM degeneration, reflecting early degeneration of occipital and parietal areas along with their WM projections ( Migliaccio et al, 2012 , 2019 ; Phillips et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Greater white matter degeneration and lower structural connectivity in non-amnestic vs. amnestic Alzheimer’s disease

Phillips,

Adluru,

Chung

et al. 2024

Front. Neurosci.

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IntroductionMultimodal evidence indicates Alzheimer’s disease (AD) is characterized by early white matter (WM) changes that precede overt cognitive impairment. WM changes have overwhelmingly been investigated in typical, amnestic mild cognitive impairment and AD; fewer studies have addressed WM change in atypical, non-amnestic syndromes. We hypothesized each non-amnestic AD syndrome would exhibit WM differences from amnestic and other non-amnestic syndromes.Materials and methodsParticipants included 45 cognitively normal (CN) individuals; 41 amnestic AD patients; and 67 patients with non-amnestic AD syndromes including logopenic-variant primary progressive aphasia (lvPPA, n = 32), posterior cortical atrophy (PCA, n = 17), behavioral variant AD (bvAD, n = 10), and corticobasal syndrome (CBS, n = 8). All had T1-weighted MRI and 30-direction diffusion-weighted imaging (DWI). We performed whole-brain deterministic tractography between 148 cortical and subcortical regions; connection strength was quantified by tractwise mean generalized fractional anisotropy. Regression models assessed effects of group and phenotype as well as associations with grey matter volume. Topological analyses assessed differences in persistent homology (numbers of graph components and cycles). Additionally, we tested associations of topological metrics with global cognition, disease duration, and DWI microstructural metrics.ResultsBoth amnestic and non-amnestic patients exhibited lower WM connection strength than CN participants in corpus callosum, cingulum, and inferior and superior longitudinal fasciculi. Overall, non-amnestic patients had more WM disease than amnestic patients. LvPPA patients had left-lateralized WM degeneration; PCA patients had reductions in connections to bilateral posterior parietal, occipital, and temporal areas. Topological analysis showed the non-amnestic but not the amnestic group had more connected components than controls, indicating persistently lower connectivity. Longer disease duration and cognitive impairment were associated with more connected components and fewer cycles in individuals’ brain graphs.DiscussionWe have previously reported syndromic differences in GM degeneration and tau accumulation between AD syndromes; here we find corresponding differences in WM tracts connecting syndrome-specific epicenters. Determining the reasons for selective WM degeneration in non-amnestic AD is a research priority that will require integration of knowledge from neuroimaging, biomarker, autopsy, and functional genetic studies. Furthermore, longitudinal studies to determine the chronology of WM vs. GM degeneration will be key to assessing evidence for WM-mediated tau spread.

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Characterization of the logopenic variant of Primary Progressive Aphasia: A systematic review and meta-analysis

Cited by 20 publications

References 111 publications

Atypical forms of Alzheimer's disease: patients not to forget

Atypical forms of Alzheimer's disease: patients not to forget

Behavioral Treatment for Speech and Language in Primary Progressive Aphasia and Primary Progressive Apraxia of Speech: A Systematic Review

Greater white matter degeneration and lower structural connectivity in non-amnestic vs. amnestic Alzheimer’s disease

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