31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
PD dementia (PDD) is associated with α-synuclein propagation, but coexistent Alzheimer's disease (AD) pathology may coexist. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Transactive response DNA-binding protein of ∼43 kDa (TDP-43), a primary pathologic substrate in tau-negative frontotemporal lobar degeneration (FTLD), is also often found in the brains of elderly individuals without FTLD and is a key player in the process of neurodegeneration in brains with and without FTLD. 4 key findings →
Design: longitudinal study Participants: 68 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a common, fatal motor neuron disorder with no effective treatment. 4 key findings →
Participants: 111 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers to determine underlying frontotemporal lobar degeneration (FTLD) tau or TAR DNA-binding protein (TDP) pathology during life are needed to advance clinical trials targeting specific FTD pathologies. 3 key findings →
Participants: 513 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Intronic expansion of the GGGGCC hexanucleotide repeat within the C9ORF72 gene causes frontotemporal dementia and amyotrophic lateral sclerosis/motor neuron disease in both familial and sporadic cases. 4 key findings →
Participants: 361 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Hypertension-associated cerebral small vessel disease is a common finding in older people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Genomic triplication of the alpha-synuclein gene (SNCA) has been reported to cause hereditary early-onset parkinsonism with dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Relating clinical symptoms to neuroanatomical profiles of brain damage and ultimately to tissue pathology is a key challenge in the field of neurodegenerative disease and particularly relevant to the heterogeneous disorders that comprise the frontotemporal lobar degeneration spectrum. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
No treatment for frontotemporal dementia (FTD), the second most common type of early-onset dementia, is available, but therapeutics are being investigated to target the 2 main proteins associated with FTD pathological subtypes: TDP-43 (FTLD-TDP) and tau (FTLD-tau). 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia with Lewy bodies (DLB) is the second most common neurodegenerative cause of dementia, behind Alzheimer's disease (AD). 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
At autopsy the striatal dopaminergic transporter is reduced. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This study traces the course of pathology in incidental and symptomatic Parkinson cases and proposes a staging procedure based upon the readily recognizable topographical extent of the lesions. 3 key findings →
Evidence: low
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Elaborating on the results, we validated one finding using a quantitative assessment of TDP-43 pathology in the granular layer of the hippocampus in FTLD-TDP brain donors with (n = 15) and without (n = 15) hallucinations. 3 key findings →
Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phospho-tau217 correlated with plasma phospho-tau181, CSF phospho-tau217 (rs = 0.68, P < 0.001), and negatively with CSF β-amyloid42/40 (rs = -0.52, P = 0.001). 4 key findings →
Design: cross-sectional Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
A diagnostic rubric is required to distinguish between limbic-predominant age-related TDP-43 encephalopathy neuropathologic change (LATE-NC) and frontotemporal lobar degeneration with TDP-43 inclusions (FTLD-TDP). 3 key findings →
Participants: 514 Evidence: low
Full summary, score breakdown and related studies → Original source
We have investigated the extent and pattern of immunostaining for the TAR DNA-binding protein, TDP-43, in 37 patients with frontotemporal lobar degeneration with ubiquitin (UBQ) pathology (FTLD-U). 4 key findings →
Participants: 37 Evidence: low
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TDP-43 (TAR-DNA binding protein) aggregates in neuronal inclusions in motoneuron disease (MND), as well as in frontotemporal lobar degeneration (FTLD) and FTLD associated with MND (FTLD-MND). 2 key findings →
Evidence: low
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Alzheimer's disease (AD) can present with distinct clinical variants. 4 key findings →
Participants: 93 Evidence: low
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This narrative review integrates longitudinal cohort studies, neuroimaging and biomarker research, and major clinical trials to examine how depression and cognitive decline interact across the dementia continuum. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Morphologically, reactive and amoeboid microglia were common in mixed DLB + AD, while homeostatic microglia with a small soma and thin processes were observed in pure DLB cases. 5 key findings →
Participants: 35 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Another proposed neuropathological feature related to TDP-43 proteinopathy in aged individuals is 'Alpha' versus 'Beta' in amygdala. 3 key findings →
Participants: 33 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Limbic-predominant age-related TDP-43 encephalopathy (LATE) is characterized by the accumulation of TAR-DNA-binding protein 43 (TDP-43) aggregates in older adults. 4 key findings →
Participants: 313 Evidence: low
Full summary, score breakdown and related studies → Original source
No asymptomatic participant and only 11% (3/27) of the symptomatic patients tested SAA positive. 5 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
Misfolded proteins accumulating in several neurodegenerative diseases (including Alzheimer, Parkinson, and Huntington diseases) can cause aggregation of their native counterparts through a mechanism similar to the infectious prion protein's induction of a pathogenic conformation onto its cellular isoform. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We identified 13 patients with a clinical diagnosis of PD who experienced dementia at least 4 years after parkinsonism onset (mean, 10.5 years) and subsequently underwent postmortem examination. 4 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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