ABCA1 is an ATP-binding cassette protein that transports cellular cholesterol and phospholipids onto high density lipoproteins (HDL) in plasma. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Genome-wide association studies (GWAS) have led to a rapid increase in available data on common genetic variants and phenotypes and numerous discoveries of new loci associated with susceptibility to common complex diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The results of several genome-wide association studies (GWASs) in the field of Alzheimer's disease (AD) have recently been published. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recently, work in cultured cells has shown that Parkin can mediate autophagy of damaged mitochondria (termed mitophagy) (Narendra et al., 2008) downstream of PINK1 (Geisler et al., 2010a; Matsuda et al., 2010; Narendra et al., 2010b; Vives-Bauza et al., 2010). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the discovery of missense mutations (A53T and A30P) in alpha-synuclein (alpha-Syn) in several families with early onset familial Parkinson's disease, alpha-Syn aggregation and fibril formation have been thought to play a role in the pathogenesis of alpha-synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The dismal success rate of clinical trials for Alzheimer's disease (AD) motivates us to develop model systems of AD pathology that have higher predictive validity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lewy body (LB) inclusions are one of the pathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The brains of patients with Alzheimer's disease (AD) invariably exhibit neuropathology in the hippocampus and entorhinal cortex when examined postmortem. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
NoD as well as PreD subjects had significant, time-dependent decreases in hippocampal and parahippocampal volume. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Although the patterns of structural and metabolic brain alterations in Alzheimer's disease are being refined and discrepancies between them are being underlined, the exact relationships between atrophy and hypometabolism are still unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In patients with idiopathic NPH, the CSF volume was significantly increased in the ventricles and decreased in the superior convexity and medial subarachnoid spaces as compared with patients with other dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Expectation of reward potentiates sensorimotor transformations to drive vigorous movements. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The dominantly inherited ataxias comprise a series of clinical phenotypes that include ataxia, dysarthria, dysmetria, and intention tremor resulting from the involvement of the cerebellum and its afferent and efferent pathways. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A considerable literature has been published on the health benefits of fish, oil-rich fish and fish oils and their constituent long-chain (LC) n-3 PUFA. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Docosahexaenoic acid (DHA), the main omega-3 fatty acid, is concentrated and avidly retained in membrane phospholipids of the nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
One of the major histopathological hallmarks of Alzheimer's disease (AD) is cerebral deposits of extracellular β-amyloid peptides. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilins (PSs) are required for Notch signaling in the development of vertebrates and invertebrates. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The use of complementary medicines, such as plant extracts, in dementia therapy varies according to the different cultural traditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
A wide range of evidence shows that cholinesterase (ChE) inhibitors can interfere with the progression of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Covarying for baseline scores, age, education, and duration of illness, the COMBO group had significantly lower mean annualized rates of deterioration in BDS and ADL scores compared with the CI (P<0.001; Cohen's dBDS=0.10-0.34 and dADL=0.23-0.46 at 1 to 2 y) and NO-RX groups (P<0.001; Cohen's dBDS=0.56-0.73 and dADL=0.32-0.48 at 1 to 2 y). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia with Lewy bodies (DLB) is common. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients treated with memantine had significantly lower NPI total scores than patients treated with placebo. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The study of molecular clock mechanisms in psychiatric disorders is gaining significant interest due to data suggesting that a misalignment between the endogenous circadian system and the sleep-wake cycle might contribute to the clinical status of patients suffering from a variety of psychiatric disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Baum, Larry PhD; Lam, Christopher Wai Kei PhD; Cheung, Stanley Kwok-Kuen MSc; Kwok, Timothy MD; Lui, Victor MRCPsych; Tsoh, Joshua MRCPsych; Lam, Linda MD, MRCPsych; Leung, Vivian FHKCPsy; Hui, Elsie FRCP; Ng, Chelsia HBSc; Woo, Jean MD; Chiu, Helen Fung Kum FRCPsych; Goggins, William B. ScD; Zee, Benny Chung-Ying PhD; Cheng, King Fai MD; Fong, Carmen Yuet Shim RN; Wong, Adrian BSc; Mok, Hazel BSc; Chow, Moses Sing Sum PharmD; Ho, Ping Chuen PhD; Ip, Siu Po PhD; Ho, Chung Shun PhD; Yu, Xiong Wen PhD; Lai, Caroline Yau Lin MMedSc; Chan, Ming-Houng FHKCPhys; Szeto, Samuel FRCP; Chan, Iris Hiu Shuen PhD; Mok, Vincent MD Author Information 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our objective was to assess the validity of the Edinburgh Cognitive and Behaviour ALS Screen (ECAS), a multi-domain screen designed to detect cognitive deficits in patients with motor disorders. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →