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Alzheimer's pathology in primary progressive aphasia
Rohrer JD, Rossor MN, Warren JD.. Neurobiology of aging, 2010-06-26
Topic: Amyloid, tau and blood-test diagnosis
Primary progressive aphasia (PPA) is a neurodegenerative disorder with language impairment as the primary feature. Different subtypes have been described and the 3 best characterized are progressive nonfluent aphasia (PNFA), semantic dementia (SD) and logopenic/phonological aphasia (LPA). Of these subtypes, LPA is most commonly associated with Alzheimer's disease (AD) pathology. However, the features of PPA associated with AD have not been fully defined. Here we retrospectively identified 14 patients with PPA and either pathologically confirmed AD or cerebrospinal fluid (CSF) biomarkers consistent with AD. Analysis of neurological and neuropsychological features revealed that all patients had a syndrome of LPA with relatively nonfluent spontaneous speech, phonemic errors, and reduced digit span; most patients also had impaired verbal episodic memory. Analysis of the pattern of cortical thinning in these patients revealed left posterior superior temporal, inferior parietal, medial temporal, and posterior cingulate involvement and in patients with more severe disease, increasing involvement of left anterior temporal and frontal cortices and right hemisphere areas in the temporo-parietal junction, posterior cingulate, and medial temporal lobe. We propose that LPA may be a "unihemispheric" presentation of AD, and discuss this concept in relation to accumulating evidence concerning language dysfunction in AD.
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APA 7th
Rohrer, J. D., Rossor, M. N., & Warren, J. D. (2012). Alzheimer's pathology in primary progressive aphasia. Neurobiology of aging. https://doi.org/10.1016/j.neurobiolaging.2010.05.020
Vancouver
Rohrer JD, Rossor MN, Warren JD. Alzheimer's pathology in primary progressive aphasia. Neurobiology of aging. 2012. doi:10.1016/j.neurobiolaging.2010.05.020. PMID: 20580129.
BibTeX
@article{rohrer2012-20580129,
author = {Rohrer, J. D. and Rossor, M. N. and Warren, J. D.},
title = {{Alzheimer's pathology in primary progressive aphasia}},
journal = {Neurobiology of aging},
year = {2012},
doi = {10.1016/j.neurobiolaging.2010.05.020},
pmid = {20580129},
url = {https://doi.org/10.1016/j.neurobiolaging.2010.05.020}
}
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Key findings
- Of these subtypes, LPA is most commonly associated with Alzheimer's disease (AD) pathology.
- However, the features of PPA associated with AD have not been fully defined.
- Analysis of neurological and neuropsychological features revealed that all patients had a syndrome of LPA with relatively nonfluent spontaneous speech, phonemic errors, and reduced digit span; most patients also had impaired verbal episodic memory.
- Analysis of the pattern of cortical thinning in these patients revealed left posterior superior temporal, inferior parietal, medial temporal, and posterior cingulate involvement and in patients with more severe disease, increasing involvement of left anterior temporal and frontal cortices and right hemisphere areas in the temporo-parietal junction, posterior cingulate, and medial temporal lobe.
Why it matters
In 14 patients with primary progressive aphasia and either pathologically confirmed Alzheimer's disease or consistent CSF biomarkers, all had a logopenic/phonological aphasia syndrome, and the authors propose it may be a unihemispheric presentation of Alzheimer's disease. This is a clinical and imaging characterization, not a treatment, cure, or prevention.
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Study details
- Participants14
- Evidence strengthLow
How this study scored 45/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 29 of the 64 points we could judge it on, which is 45 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Neurobiology of aging) |
| Journal's citation record | — / 4 | No journal record from OpenAlex — left out of this score |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 1 / 5 | 2012 — within 20 year(s) of the newest study here |
| Sample size | 1 / 4 | 14 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | — / 7 | No citation count (OpenAlex dates this DOI to 2010, the record says 2012; OpenAlex values not used) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | 2 / 6 | Cited by 8 other studies in this library |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 20580129) |
| Free to read | 2 / 2 | Free to read |
| Points | 29 / 64 | Scored on 12 of 20 parts. We have no data for the rest, so they are left out: 29 of the 64 points we could judge it on is 45 out of 100. |
| Total | 45 / 100 | — |
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