FUS gene mutations were recently identified in familial amyotrophic lateral sclerosis (ALS). 4 key findings →
Evidence: low
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Research
30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Amyotrophic lateral sclerosis (ALS), a common late-onset neurodegenerative disease, is associated with fronto-temporal dementia (FTD) in 3-10% of patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) refers to a group of progressive neurodegenerative disorders with different pathological signatures, genetic variability and complex disease mechanisms, for which no effective treatments exist. 4 key findings →
Evidence: low
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Parkinson's disease (PD) is a common neurodegenerative disease associated with accumulation of misfolding proteins and increased neuroinflammation, which may further impair the glymphatic system. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Comorbidity indices for patients with cognitive impairment increased during the 6-year study period, especially after the index. 5 key findings →
Participants: 2,711 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
NfL holds potential as a blood-based biomarker for symptomatic genetic FTD carriers, with moderate accuracy to distinguish PPD from mild forms including C9orf72 . 3 key findings →
Participants: 474 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the cohort, 39.2% (67/171) tested positive by α-syn SAA. α-syn SAA positivity was more frequently detected alone than in combination with biomarkers of AD pathology (25.1% vs. 14.0%). α-syn SAA+ status was independently associated with higher odds of fluctuating cognition (OR 2.99, 95%CI 1.46–6.25, p = 0.012), visual hallucinations (OR 2.41, 95%CI 1.24–4.75, p = 0.027), extrapyramidal signs (OR 4.57, 95%CI 2.35–9.11, p < 0.001) and akinetic mutism (OR 3.77, 95%CI 1.22–12.82, p = 0.038). 5 key findings →
Participants: 171 Evidence: moderate
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A total of 110 patients were identified. 5 key findings →
Participants: 110 Evidence: low
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are progressive adult-onset neurodegenerative diseases with overlapping pathological and genetic origins. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a defining feature of Lewy body disease: its timing and onset distinguish different clinical diagnoses, and its effect on quality of life is profound. 1 key finding →
Participants: 108 Evidence: low
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Males were more likely than females to present with two or more core DLB clinical features 2 years prior to obtaining a diagnosis of dementia. 5 key findings →
Design: longitudinal study Evidence: moderate
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In the central Lewy body diseases (LBDs) Parkinson's disease and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests, substantial central neurodegeneration has already occurred. 5 key findings →
Design: longitudinal study Evidence: moderate
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All included PD patients were cognitively normal at baseline and had 6 years of follow-up assessments available for cognitive status. 5 key findings →
Design: longitudinal study Participants: 47 Evidence: moderate
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= 0.015). In this autopsy-confirmed cohort, seizure susceptibility was associated with advanced tau pathology and CAA in AD. 4 key findings →
Design: cohort study Evidence: moderate
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49/100
Adult-onset neurodegenerative diseases affect millions and negatively impact health care systems worldwide. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We screened 3,809 articles and identified 31 eligible studies. 2 key findings →
Design: systematic review Evidence: high
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Sleep disruption and other circadian rhythm disturbances are frequently seen in dementia patients. 2 key findings →
Participants: 30 Evidence: low
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48/100
Intravitam PET and post-mortem studies revealed more pronounced cortical atrophy, elevated cortical and limbic Lewy pathologies (with APOE ε4), apart from higher prevalence of Alzheimer pathology in DLB than PDD. 2 key findings →
Evidence: low
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Epidemiologic studies indicate that elderly women are at higher risk for Alzheimer disease compared to men. 3 key findings →
Evidence: low
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Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). 1 key finding →
Evidence: low
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48/100
Investigation of dopaminergic transporter loss in vivo using (123)I-N-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl) nortropane single photon emission computed tomography has been widely used as a diagnostic aid in Lewy body disease. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
48/100
Contrary to some prior reports, behavioral variant frontotemporal dementia (bv-FTD) patients who progress over time are typically impaired on executive tasks at first presentation, although an important minority of true FTD patients perform normally. 3 key findings →
Evidence: low
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To determine the prevalence of depression in Parkinson disease (PD) we evaluated 55 consecutive patients without dementia and 31 of their spouses. 4 key findings →
Evidence: low
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Microglia-derived inflammatory neurotoxins play a principal role in the pathogenesis of neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and HIV-associated dementia; chief among these is reactive oxygen species. 2 key findings →
Evidence: low
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This study provides pathological validation that the new criteria assist with separating PPA cases with AD pathology into the new lv-PPA syndrome and found that a number of diagnostic clinical features (disinhibition, food preferences and naming) did not assist in discriminating the different FTD syndromes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
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.
- Comparison of Integrated Outpatient Palliative Care With Standard Care in Patients With Parkinson Disease and Related Disorders: A Randomized Clinical Trial
- Neurofilament light chain and α-synuclein RT-QuIC as differential diagnostic biomarkers in parkinsonisms and related syndromes
- Alzheimer disease with amygdala Lewy bodies: a distinct form of alpha-synucleinopathy
- White matter hyperintensities precede other biomarkers in GRN frontotemporal dementia
- Impact of coexistent Alzheimer pathology on the natural history of Parkinson's disease
- Priority setting partnership to identify the top 10 research priorities for the management of Parkinson's disease
- Hallucinations in Parkinson disease
- Excessive daytime sleepiness and sudden-onset sleep in Parkinson disease: a survey by the Canadian Movement Disorders Group
- Ageing and Parkinson's disease: substantia nigra regional selectivity
- TDP-43 pathology in Alzheimer's disease, dementia with Lewy bodies and ageing
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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