27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The double dissociation in performance on semantic memory and attention/executive function clearly separated the temporal and frontal variants of FTD and aids the early differentiation of FTD from AD. 3 key findings →
Evidence: low
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A temporoparietal pattern of atrophy on MRI in patients with progressive fluent aphasia and relatively preserved processing speed is suggestive of underlying Alzheimer disease pathology rather than frontotemporal lobar degeneration with ubiquitin-only immunoreactive changes. 3 key findings →
Participants: 216 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disease-specific patterns of functional network topology and connectivity alterations were observed in patients with EOAD and bvFTD. 3 key findings →
Participants: 37 Evidence: low
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Intracytoplasmic aggregation of alpha-synuclein protein as Lewy bodies in the brainstem neurons is diagnostic for Parkinson's disease, whereas if this process also occurs in the cortical neurons, it is considered pathognomonic for dementia with Lewy bodies. 2 key findings →
Participants: 904 Evidence: low
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Disinhibition is a common behavioural symptom in frontotemporal dementia but its neural correlates are still debated. 3 key findings →
Participants: 14 Evidence: low
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Dementia with Lewy bodies is the second most common form of neurodegenerative dementia, yet scarce evidence is available about its prognosis and natural history, which are crucial to inform clinical practice and research. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is considerable variation in the phenotypic appearance of individuals with idiopathic Parkinson's disease (PD), which may translate into differences in disease progression in addition to underlying disease etiology. 5 key findings →
Participants: 162 Evidence: low
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Parkinsonism is a common disease among the elderly; its incidence increases steeply with advancing age and is consistently higher in men. 1 key finding →
Evidence: low
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Prospective studies have shown that although the beneficial effects of this procedure are maintained at 5 years, axial motor features and cognitive decline may occur in the long term after the implants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The temporal variant of frontotemporal dementia follows a characteristic cognitive and behavioral progression that suggests early spread from one anterior temporal lobe to the other. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The clinical syndrome of pure akinesia has most often been associated with progressive supranuclear palsy (PSP) and is characterized by difficulty initiating gait and "freezing" during walking, writing and speaking. 1 key finding →
Participants: 749 Evidence: low
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Relative to healthy controls, and after accounting for nonverbal executive performance, patients with bvFTD showed deficits of noun and verb naming and single word comprehension, diminished spontaneous propositional speech, and deterioration in naming performance over time. 3 key findings →
Participants: 24 Evidence: moderate
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This study demonstrated the use of speech measures in the identification of those with an oral-motor deficit, and showed the usefulness of performing a relatively simple reading test to assess speech versus pause behaviors across the ALS-FTD disease continuum. 3 key findings →
Participants: 136 Evidence: low
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This multimodal approach enhanced the system's performance and provided a clinically informative method for neuroimaging analysis. 1 key finding →
Participants: 44 Evidence: low
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So-called idiopathic rapid eye movement (REM) sleep behaviour disorder (RBD), formerly seen as a rare parasomnia, is now recognized as the prodromal stage of an α-synucleinopathy. 5 key findings →
Evidence: low
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Subtyping PPA helps to predict AD versus frontotemporal lobar degeneration pathology at the group level. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
As a more complete picture of the clinical phenotype of Parkinson's disease emerges, non-motor symptoms have become increasingly studied. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The discovery that repeat expansions in the C9orf72 gene are a frequent cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has revolutionized our understanding of these diseases. 1 key finding →
Evidence: low
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The authors studied the accuracy of clinical diagnosis of idiopathic PD (IPD) in 100 consecutive clinically diagnosed cases that came to neuropathological examination. 1 key finding →
Evidence: low
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α-Synuclein species contained in PD-derived LB are pathogenic and have the capacity to initiate a PD-like pathological process, including intracellular and presynaptic accumulations of pathological α-synuclein in different brain areas and slowly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration. 2 key findings →
Evidence: low
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Gene defects play a major role in the pathogenesis of degenerative disorders of the nervous system. 3 key findings →
Evidence: low
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Increased awareness of cognitive and behavioural change in amyotrophic lateral sclerosis has been driven by various clinic-based and population-based studies. 5 key findings →
Evidence: low
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The tau gene has been found to be the locus of dementia with rigidity linked to chromosome 17. 5 key findings →
Evidence: low
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The amygdala exhibits significant pathological changes in Parkinson's disease, including atrophy and Lewy body (LB) formation. 2 key findings →
Evidence: low
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These findings confirm that MCI is associated with widespread cortical atrophy. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
10 of the 1,021 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,780 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,034 records (3.7% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →