27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer's disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders, such as Alzheimer's disease (AD), Parkinson's disease (PD) and frontotemporal dementias (FTD), are considered distinct entities, however, there is increasing evidence of an overlap from the clinical, pathological and genetic points of view. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta (Aβ) is a peptide of 39-43 amino acids found in large amounts and forming deposits in the brain tissue of patients with Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most prevalent tauopathy and cause of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by cognitive decline, brain atrophy due to neuronal and synapse loss, and formation of two pathological lesions: extracellular amyloid plaques, composed largely of amyloid-beta peptide (Aβ), and neurofibrillary tangles formed by intracellular aggregates of hyperphosphorylated tau protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Single, severe traumatic brain injury (TBI) which elevates CNS amyloid, increases the risk of Alzheimer's disease (AD); while repetitive concussive and subconcussive events as observed in athletes and military personnel, may increase the risk of chronic traumatic encephalopathy (CTE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Altered synaptic function is considered one of the first features of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent type of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The early stages of Alzheimer's disease are characterised by impaired synaptic plasticity and synapse loss. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Little is known about how changes in DNA methylation mediate risk for human diseases including dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The prefrontal cortex and medial temporal lobe are particularly vulnerable to the effects of aging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For more than two decades, there have been extensive studies of experience-based neural plasticity exploring effective applications of brain plasticity for cognitive and motor development. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A lighting intervention, tailored to increase daytime circadian stimulation, can be used to increase sleep quality and improve behavior in patients with ADRD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic heart failure (CHF) is the leading cause of hospitalization for those over the age of 65 and represents a significant clinical and economic burden. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Place of death of older people who died from a dementia-related disease differs substantially between countries, which might point to organizational differences in end-of-life care provision. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is difficult to define what constitutes high-quality end-of-life care for people with dementia from the perspective of family carers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Future palliative care policy decisions in Ireland must consider the rapidly aging Irish population with the accompanying increase in deaths from cancer, dementia, and neurodegenerative disease and associated palliative care need. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ongoing change in long-term care from institutional care to housing services causes major challenges to the continuity of end-of-life care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
International experts selected a set of 23 QIs for the organisation of palliative care. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Scientific evidence continues to demonstrate the linkage of vascular contributions to cognitive impairment and dementia such as Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive impairment and memory dysfunction following stroke diagnosis are common symptoms that significantly affect the survivors' quality of life. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Presenilin 1 (PSEN1) encodes the catalytic subunit of γ-secretase, and PSEN1 mutations are the most common cause of early onset familial Alzheimer's disease (FAD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An early substantial loss of basal forebrain cholinergic neurons (BFCNs) is a constant feature of Alzheimer's disease (AD) and is associated with deficits in spatial learning and memory. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This biomarker discrepancy is likely due to overexpression of amyloid precursor protein in the transformed cellular models. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The high Aβ42/Aβ40 production ratio is a hallmark of familial Alzheimer's disease, which can be caused by mutations in the amyloid precursor protein (APP). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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.
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 →