Cholinergic deficits might contribute to vascular cognitive impairment. 4 key findings →
Participants: 86 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
We found up to 270-fold genetic enrichment between FTD and RA, up to 160-fold genetic enrichment between FTD and UC, up to 180-fold genetic enrichment between FTD and T1D, and up to 175-fold genetic enrichment between FTD and CeD. 5 key findings →
Design: meta-analysis Participants: 192,886 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Patients trained with CoRe showed a better evolution of cognitive decline, while untreated patients tended to get worse over time. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Neuropathology cases included 46 Parkinson's disease and 10 dementia with Lewy bodies, and clinical cases included 173 Parkinson's disease, and 64 controls. 5 key findings →
Design: cohort study Participants: 46 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB. 5 key findings →
Design: longitudinal study Participants: 222 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Sleep apnea (SA) is potentially a modifiable risk factor for dementia. 5 key findings →
Design: meta-analysis Participants: 1,333,424 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
White matter hyperintensities (WMH) are the most common brain-imaging feature of cerebral small vessel disease (SVD), hypertension being the main known risk factor. 1 key finding →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Quetiapine was well-tolerated and did not worsen parkinsonism. 3 key findings →
Participants: 23 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
70/100
We have demonstrated that three baseline measures, namely, age >or=72 years, semantic fluency less than 20 words in 90 s and inability to copy an intersecting pentagons figure, are significant predictors of dementia risk, thus validating our previous findings. 5 key findings →
Design: cross-sectional Participants: 126 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Abnormal aggregates of the synaptic protein, α-synuclein, are the dominant pathology in syndromes known as the synucleinopathies. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
APOE ε4 may influence the association between WMH and cognitive performance in AD and DLB. 5 key findings →
Design: meta-analysis Participants: 167 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Between 2001, and 2012, we identified 243 611 incident cases of dementia, 31 577 cases of Parkinson's disease, and 9247 cases of multiple sclerosis. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
70/100
Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results. 4 key findings →
Design: longitudinal study Participants: 281 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 143 iRBD participants (110 male, 67.7 ± 8.0 years) were included. 5 key findings →
Design: cohort study Participants: 2,004 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The CDR+NACC FTLD global score interacted with time on battery percentage such that participants with prodromal or symptomatic FTLD demonstrated less change in battery percentage throughout the day (a proxy for less smartphone use) than clinically normal participants (P<.001 in both cases). 4 key findings →
Design: longitudinal study Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CL was associated with syndromic (F = 4.42, p = 0.014) and etiological diagnosis (F = -12.66, p < 0.001), with Alzheimer's disease (AD) patients showing the highest amyloid burden (62.9 ± 27.5), followed by dementia with Lewy bodies (DLB) (25.3 ± 35.5) and cardiovascular disease (CVD) (16.7 ± 24.5), and finally frontotemporal lobe degeneration (FTLD) (5.0 ± 17.22, t = -12.66, p < 0.001). 4 key findings →
Design: longitudinal study Participants: 157 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Huntington's Disease (HD) is a severely debilitating neurodegenerative disorder in which sufferers exhibit different combinations of movement disorders, dementia, and behavioral or psychiatric abnormalities. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
The present study showed that higher educational levels were related to better general cognitive function, executive function, memory, and information processing speed in PD patients, whereas no significant association was showed between educational levels and visuospatial function, language in PD patients. 4 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Vascular dementia (VD) is a neurocognitive disorder whose precise definition is still up for debate. 1 key finding →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
The primary outcome was difference in the change in Neuropsychiatric Inventory apathy scores for oxytocin versus placebo periods in the per-protocol population after 6 weeks of treatment. 2 key findings →
Design: phase-2-trial Participants: 94 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
69/100
Identifying concomitant Lewy body (LB) pathology through seed amplification assays (SAA) might enhance the diagnostic and prognostic work-up of Alzheimer's disease (AD) in clinical practice and trials. 2 key findings →
Design: cohort Participants: 795 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The management of symptomatic orthostatic hypotension, autonomic symptoms and depression, and the encouragement of physical activity may provide the core elements for the most fruitful strategy to reduce falls in people with dementia. 2 key findings →
Participants: 179 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
69/100
We conclude that there is evidence supporting the hypothesis that physical activity is likely to prevent the development of VaD, and should be highlighted as part of secondary prevention programmes in people at risk for cerebrovascular disease. 4 key findings →
Design: meta-analysis Participants: 1,378 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Dementia is a key part of survival in Parkinson disease and must be planned for in services for this condition. 1 key finding →
Design: cohort study Participants: 140 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We have carried out a systematic review of the case files of 242 donors with pathologically verified Parkinson's disease at the Queen Square Brain Bank for Neurological Disorders in an attempt to corroborate the data-driven subtype classification proposed by Lewis and colleagues (Heterogeneity of Parkinson's disease in the early clinical stages using a data driven approach. 4 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 2,674 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.
- Expression of Nrf2 in neurodegenerative diseases
- Alice in Wonderland Syndrome in dementia with Lewy bodies: a case report exploring visual cognition dysfunction
- Mutations in the FUS/TLS Gene on Chromosome 16 Cause Familial Amyotrophic Lateral Sclerosis
- Shared genes and pathways in dementia: Insights from genome-wide association studies
- Electroencephalographic Finding in Idiopathic REM Sleep Behavior Disorder
- Interleukin-1β, interleukin-1 receptor antagonist, interleukin-6, interleukin-10, and tumor necrosis factor-α levels in CSF and serum in relation to the clinical diversity of Parkinson's disease
- Bidirectional transcripts of the expanded C9orf72 hexanucleotide repeat are translated into aggregating dipeptide repeat proteins
- Application of mini-mental state examination and Montreal Cognitive Assessment in the diagnosis of dementia with Lewy bodies and Alzheimer’s disease
- The spectrum of disease in chronic traumatic encephalopathy
- Clinical subtypes of chronic traumatic encephalopathy: literature review and proposed research diagnostic criteria for traumatic encephalopathy syndrome
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →