High levels of amyloid-β peptide (Aβ) have been related to Alzheimer's disease pathogenesis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Morphological changes of dendritic spines are strongly associated with synaptic development and synaptic plasticity, which underlies learning and memory. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this study was to investigate the effects of netrin-1 (NT-1) on amyloid-beta (Aβ)-induced impairments in learning-memory and synaptic plasticity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synapse loss is a key feature of dementia, but it is unclear whether synaptic dysfunction precedes degenerative phases of the disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cholinergic dysfunction has been associated with cognitive abnormalities in a variety of neurodegenerative and neuropsychiatric diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction due to the disrupting binding of amyloid beta (Aβ) and tau oligomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Proteolytic processing of amyloid precursor protein (APP) C-terminal fragments (CTFs) by γ-secretase underlies the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Damaged or aggregated proteins and organelles accumulate with age and contribute to various age-related pathologies including Alzheimer, Parkinson or Huntington diseases. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Protein dyshomeostasis is the common mechanism of neurodegenerative diseases such as Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria are pivotal organelles in eukaryotic cells. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Protein homeostasis, or proteostasis, has an important regulatory role in cellular function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Despite the progress made in the understanding of the etiology, neuropathophysiology, and treatment of different types of dementia, such disorders continue to pose huge health problems worldwide. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of personhood developed by Tom Kitwood highlights that the experience of dementia has relational dimensions that transcend the neurodegenerative impacts of the condition. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We provide a review of the current literature and discuss our own care practices. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-four staff members completed the survey and reported positive perspectives about the training, use of the program, and benefits for PWD and themselves. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sixteen states license or certify dementia care units within RC/AL settings. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Data were analysed using thematic analysis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
A one percentage point reduction in elderspeak costs $6.75 per staff member with average baseline elderspeak usage. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Dementia will become more common as the population ages. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
With the growing care needs for the older population at the end of their lives, there has been a substantial increase in attention to the management of the patient with dementia in hospice and palliative care services. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
NPs care for patients with chronic diseases such as heart failure, chronic obstructive pulmonary disease, cancer, and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because of the rapidly growing older population and increases in longevity, rates of dementia have been rising. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia and fragility fractures are two conditions that pose significant morbidity and mortality to the elderly population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biomarkers of the molecular pathology underpinning dementia syndromes are increasingly recognized as crucial for diagnosis and development of disease-modifying treatments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →