Cholinergic deficiency is the most consistent transmitter system abnormality in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Agitation is common and distressing in patients with Alzheimer-type dementia, but safe, effective treatments remain elusive. 1 key finding →
Participants: 200 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Seventy-one patients completed the trial. 5 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
We found no statistically significant differences in UPDRS scores, plasma BDNF levels or H(1)-MRS measures. 3 key findings →
Participants: 119 Evidence: low
Full summary, score breakdown and related studies → Original source
The amyloid hypothesis suggests that the progressive accumulation and deposition of central nervous system (CNS) amyloid with aging is the proximate cause of Alzheimer's disease (AD). 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
SBME produced significant improvement on mental control, logical memory and paired associated learning during the 12-week drug therapy. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
This single-blind, placebo controlled study reports on the effects of administering three acute doses of nicotine (0.4, 0.6 and 0.8 mg) subcutaneously to a group of Alzheimer's disease (DAT) patients (n = 22), young adult controls (n = 24), and normal aged controls (n = 24). 3 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source
GBA-related PD (GBA-PD) patients have higher risk of dementia and reduced survival than non-carriers. 3 key findings →
Design: open-label trial Evidence: low
Full summary, score breakdown and related studies → Original source
Drug development for Alzheimer disease and other neurodegenerative dementias, including frontotemporal dementia, has experienced a long history of phase 2 and phase 3 clinical trials that failed to show efficacy of investigational drugs. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Regions were heterogeneous at baseline. At baseline, disease severity as measured by ADAS-cog11, ADCS-ADL, and CDR-SB was numerically worse for Eastern Europe/Russia compared with other regions. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
The Alzheimer disease (AD) neuropathological hallmarks amyloid β (Aβ) and tau neurofibrillary (NF) pathology have been reported in the olfactory bulb (OB) in aging and in different neurodegenerative diseases, which coincides with frequently reported olfactory dysfunction in these conditions. 1 key finding →
Design: clinical trial Evidence: moderate
Full summary, score breakdown and related studies → Original source
Behavioural troubles due to frontotemporal dementia (FTD) are difficult to treat. 3 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Curcumin possesses many properties which may prevent or ameliorate pathological processes underlying age-related cognitive decline, dementia or mood disorders. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
The Clinicaltrials.gov database demonstrates that relatively few clinical trials are undertaken for AD therapeutics, considering the magnitude of the problem. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Psychosis and agitation are among the most distressing neuropsychiatric symptoms (NPSs) of Alzheimer's disease (AD), linked to faster disease progression and earlier admission to nursing homes. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Lecanemab is a humanized monoclonal antibody directed against human soluble amyloid-β aggregates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Efforts to develop new therapies to combat Alzheimer's disease suffer from extraordinarily high failure rates that make it difficult to justify continued investment in the field. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The patent introduces a class of agents that target amyloid aggregation, and subsequently, reduce amyloid β-oligomer neurotoxicity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this multicenter study, the clinical efficacy of citalopram was investigated in 98 patients with moderate AD/SDAT or VD using a combined double-blind and open technique with placebo and citalopram. 2 key findings →
Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Physostigmine (0.25 mg-1 mg), arecoline (2 and 4 mg) and saline were administered intravenously over 30 minutes in a randomized double blind design to 11 patients with a clinical diagnosis of Alzheimer presenile dementia. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
41/100
In mammals, a central circadian clock, located in the suprachiasmatic nuclei (SCN) of the hypothalamus, tunes the innate circadian physiological rhythms to the ambient 24 h light-dark cycle to invigorate and optimize the internal temporal order. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
RECENT FINDINGS: In a large autopsy series from a national consortium, multiple neuropathologies of dementia subtypes were common and increased severity of specific NPS during life was associated with greater severity of neuropathology across diagnoses. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Frailty is a critical intermediate status of the aging process with a multidimensional and multisystem nature and at higher risk for adverse health-related outcomes, including falls, disability, hospitalizations, institutionalization, mortality, dementia, and Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There are currently 24 agents in 36 trials in phase III of AD drug development. 5 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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