Alzheimer's disease is the commonest cause of dementia in the elderly, but its pathological determinants are still debated. 5 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.
A hallmark of Alzheimer disease (AD) is the accumulation of the amyloid-β (Aβ) peptide in the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our case studies highlight that not all athletes with history of repeated concussions and neurological symptomology present neuropathological changes of CTE. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common type of age-related dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-brain barrier (BBB) regulates transport of various molecules and maintains brain homeostasis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Methylation is a post-translational modification that can affect numerous features of proteins, notably cellular localization, turnover, activity, and molecular interactions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The Niemann-Pick disease group is now divided into two distinct entities: (1) acid sphingomyelinase-deficient Niemann-Pick disease (ASM-deficient NPD) resulting from mutations in the SMPD1 gene and encompassing type A and type B as well as intermediate forms; (2) Niemann-Pick disease type C (NP-C) including also type D, resulting from mutations in either the NPC1 or the NPC2 gene. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our purpose was to determine whether the neurochemistry of the primary motor cortex measured with proton magnetic resonance spectroscopy, and its volume, were associated with gait performance while single and dual-tasking in mild cognitive impairment. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regardless of the dementia stage, many nursing home residents develop serious clinical complications and symptoms in the last phase of life, posing major challenges to the provision of optimum end-of-life care. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Communication regarding care is rarely patient driven and more often professional caregiver or family driven. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Approaches to palliative care that were originally developed for people with cancer are now being adopted for people with dementia, as a response to many reports of poor-quality care for people with dementia at the end of life. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
These are not problems distinct to palliative care, but they may have different origins and explanations compared to other areas of health care. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Loss of memory is among the first symptoms reported by patients suffering from Alzheimer's disease (AD) and by their caretakers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Our findings support the theory that alterations in hippocampal glutamate levels potentially account for structural deficits in the hippocampus observed in schizophrenia neuroimaging studies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Idiopathic normal pressure hydrocephalus (INPH) is a syndrome of ventriculomegaly, gait impairment, cognitive decline and incontinence that occurs in an elderly population prone to many types of comorbidities. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological amino-acid substitutions in the amyloid precursor protein (APP) and chemical γ-secretase modulators affect the processing of APP by the γ-secretase complex and the production of the amyloid-beta peptide Aβ42, the accumulation of which is considered causative of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Treatment of Alzheimer's disease (AD) is significantly hampered by the lack of easily accessible biomarkers that can detect disease presence and predict disease risk reliably. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Substances produced throughout the body are detectable in the blood, which is the most common biological fluid used in clinical testing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the search for new genes in Alzheimer's disease, classic linkage-based and candidate-gene-based association studies have been supplanted by exome sequencing, genome-wide sequencing (for mendelian forms of Alzheimer's disease), and genome-wide association studies (for non-mendelian forms). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ATP-binding cassette transporter A7 (ABCA7) is expressed in the brain and has been detected in macrophages, microglia, and neurons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The UPR is activated in disease affected regions in PSP and the genetic evidence shows that this activation increases risk for PSP and is not a protective response. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[(18)F]T807 demonstrates high affinity and selectivity to PHF-tau as well as favorable in vivo properties, making this a promising candidate as an imaging agent for AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The findings suggest that CA1 measurement is more sensitive than global hippocampal volumetry to detect structural changes at the pre-dementia stage, although the predominance of CA1 atrophy does not appear to be specific to AD pathophysiological processes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
However, other evidence suggests that the region is highly heterogeneous and may play a direct role in regulating the focus of attention. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The earliest detectable change in Alzheimer's disease (AD) is the buildup of amyloid plaque in the brain. 1 key finding →
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 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 →