30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
A total of 798 patients (154 with probable DLB and 644 with AD) were included, and the mean age was 81.4 years (SD 6.33). 5 key findings →
Design: cross-sectional Participants: 798 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In contrast, patients with LB pathology alone, in the absence of AD biomarker positivity, had less overall cognitive impairment but more focal dysexecutive and visuospatial deficits. 5 key findings →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Clinical and neuropathological criteria forfrontotemporal dementia * Early loss of insight into the fact that the altered condition is due to a pathological change of own mental state. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This systematic review aims to elucidate the neuropathological basis of the HIDA and psychosis domains, exploring whether distinct proteinopathies and neural circuit dysfunctions are associated with these symptoms. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We report five patients with a stereotyped clinical syndrome characterized by fluent dysphasia with severe anomia, reduced vocabulary and prominent impairment of single-word comprehension, progressing to a stage of virtually complete dissolution of the semantic components of language.
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Beta-amyloid (Aβ 1-42 ) triggers the phosphorylation of tau protein in Alzheimer's disease (AD), but the relationship between phosphorylated tau (p-tau) and Aβ 1-42 in the blood is not elucidated. 4 key findings →
Participants: 62 Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) has been suggested as a biomarker for reactive astrogliosis. 2 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source
This was then correlated with overall cortical flortaucipir PET and PiB PET standardized uptake value ratio (SUVr). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The C9orf72 expansion is a common cause of ALS and FTLD, but not of AD or PD. 4 key findings →
Participants: 520 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
One-third of the 149 people recruited 15 to 18 years ago in the Sydney Multicenter Study of Parkinson's disease have survived. 2 key findings →
Participants: 15 Evidence: low
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The correct diagnosis of Parkinson's disease is important for prognostic and therapeutic reasons and is essential for clinical research. 1 key finding →
Evidence: low
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Deficits in cholinergic function have been postulated to cause delirium and cognitive decline. 1 key finding →
Evidence: low
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Severe, and often fatal, neuroleptic sensitivity may occur in elderly patients with confusion, dementia, or behavioural disturbance. 3 key findings →
Participants: 21 Evidence: low
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Synucleinopathies are clinically and pathologically heterogeneous disorders characterized by pathologic aggregates of α-synuclein in neurons and glia, in the form of Lewy bodies, Lewy neurites, neuronal cytoplasmic inclusions, and glial cytoplasmic inclusions. 2 key findings →
Evidence: low
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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
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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
Full summary, score breakdown and related studies → Original source Free full text
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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10 of the 1,072 studies in this tag that have a study page, 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events