27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
FUS is a nuclear RNA-binding protein, and its cytoplasmic aggregation is a pathogenic signature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) encompasses a spectrum of clinical syndromes characterized by progressive executive, behavioural and language dysfunction. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients at late stage Parkinson's disease (PD) develop several motor and nonmotor complications, which dramatically impair their quality of life. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) is a dementia syndrome characterized by peculiar behavioral changes arising from frontotemporal involvement and distinct from Alzheimer's disease (AD). 4 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Since its first description by Charcot, amyotrophic lateral sclerosis (ALS) has been classified as a single neurodegenerative disease involving motor neurons. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
At the initial visit, the mean age of individuals with DLB was 80.8 (5.8) years; their mean Mini-Mental State Examination score was 20.6 (5.1). 5 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
< .01). All patient groups were also impaired on AVLT encoding, TMT-B and TMT B/A. Social and non-social neurocognitive functions differed between groups, with specific impairments in processing speed in VaD, emotion recognition in bv-FTD and memory retrieval in AD, and memory encoding and cognitive control impaired in all three groups. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gait disturbances (odds ratio (OR) = 19.32; p = 0.01), visual-spatial complaints (OR = 6.06; p = 0.03), and visual hallucinations (OR = 31.06; p = 0.002) predicted DLB compared to AD, along with better memory (OR = 3.42; p = 0.003), naming (OR = 3.35; p = 0.002), and worse processing speed (OR = 0.51; p = 0.01). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The spectral analysis of the resting-state eyes-closed electroencephalographic (rsEEG) activity typically shows abnormal delta (< 4 Hz), theta (4-7 Hz), and alpha (8-12 Hz) power in older patients with cognitive deficits due to progressive neurodegenerative diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Diagnosis of LBD had high specificity but low sensitivity, with fewer than half of autopsy-confirmed cases having received an LBD diagnosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In plasma, most complement analytes were not significantly different between spFTD and HC; the exceptions were C4 and FB, significantly decreased in spFTD vs HC ( p = 0.0192 and p = 0.0181, respectively), suggesting complement consumption in classical and alternative pathways. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A descriptive study using a transversal national online survey to evaluate the prevalence and characteristics of behavioral and psychological symptoms (BPSD) of dementia with Lewy bodies (DLB), and specifically, the perpetration of violent acts against primary caregivers. 196 responses, obtained in one month, were analyzed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Proteinopathies such as Alzheimer, Parkinson, and Huntington diseases, where aberrant proteins spread throughout the brain during disease progression, may share a molecular basis and mechanisms of propagation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a common feature in Parkinson's disease (PD) and is considered to be the result of limbic and cortical Lewy bodies and/or Alzheimer changes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Progressive multifocal leukoencephalopathy, a formerly rare disease that chiefly occurred in persons with underlying lymphoma and chronic lymphocytic leukemia, is now seen with increasing frequency in the era of acquired immunodeficiency syndrome. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
An increasing number of individuals in our population are surviving to over 90 years and a subset is at risk for developing dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes (T2D) and dementia frequently co-occur, yet the biological mechanisms underlying this comorbidity remain incompletely understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To investigate alterations in resting-state electroencephalogram (EEG) microstates across the cognitive spectrum of Parkinson's disease (PD) and to evaluate their utility as electrophysiological biomarkers of cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
26% of the participants experienced delirium prior to diagnosis of DLB, with one participant experiencing multiple episodes in the 24 months before diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lewy bodies, the pathological hallmark of dementia with Lewy bodies (DLB), are large juxtanuclear inclusions of aggregated alpha-synuclein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several neurodegenerative diseases are typified by intraneuronal alpha-synuclein deposits, synaptic dysfunction, and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia is a neurological disorder characterised by personality changes, deterioration of memory and executive functions as well as stereotypical behaviour. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Lewy body disease (LBD) are the most common causes of dementia in the elderly population. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal degeneration (CBD) is a rare, progressive neurodegenerative disorder with onset in the 5(th) to 7(th) decade of life. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alterations in synaptic protein stoichiometry may contribute to neocortical synaptic dysfunction in Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 →