29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
An expanded hexanucleotide repeat in the C9orf72 gene is the most common genetic cause of frontotemporal dementia and amyotrophic lateral sclerosis (c9FTD/ALS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The daily rhythm in serum melatonin levels was measured in patients with dementia of the degenerate type (Alzheimer's disease, Pick's disease and senile dementia of the Alzheimer type) by radioimmunoassay. 2 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
When assessed via instrumentation, swallowing abnormalities are found in many patients with FTLD. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
Our study shows that an intensive educational training and adaptation on non-invasive ventilation, when performed in a hospital multidisciplinary setting, increases compliance and tolerance over time, even in those patients with severe bulbar impairment. 2 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
As our population ages, therapies increase, and the number of individuals living with advanced PD and related disorders grows, so too does the imperative to recognize and address the palliative care needs of such patients and families. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hippocampal atrophy is not only a characteristic of Alzheimer's disease but also occurs in FTLD. 5 key findings →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
Diffusion tensor measurements correlate better with cognition than conventional MRI measures. 3 key findings →
Participants: 36 Evidence: low
Full summary, score breakdown and related studies → Original source
Both CSF tau and CSF phosphotau were increased in probable AD compared with FTD (p<0.001), SAE (p<0.001), PD (p<0.001), and controls (p<0.001). 4 key findings →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source
The CSF Abeta42/Abeta40 ratio improves differentiation of AD patients from VaD, DLB and non-AD dementia patients, when compared to Abeta42 alone, and is a more easily interpretable alternative to the combination of Abeta42, p-tau and t-tau when differentiating AD from either FTD or non-AD dementia. 4 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results support further efforts to prospectively validate the use of Q Abeta42/p-tau as a biomarker to discriminate between AD and VaD. 2 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based tests for the differential diagnosis of Alzheimer's disease (AD) are under intensive investigation and have shown promising results with regard to Abeta40 and Abeta42 peptide species in incipient AD. 2 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
CogState and standard neuropsychological task scores were significantly lower for dementia participants than that of the nondementia groups (P < .05), with a single CogState test distinguishing control from MCI participants, but minimal differentiation existing between dementias using the CogState. 2 key findings →
Participants: 37 Evidence: low
Full summary, score breakdown and related studies → Original source
In established dementia, administration of the CogState tasks appears sensitive to cognitive impairment in dementia. 1 key finding →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source
Although the frequency of the mutations is low in our series (4 of 188 patients [2%]), our results, similar to those already reported, support a direct pathogenic role of p62 in different types of FTD. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Currently, there is no disease-modifying treatment available for Alzheimer's and Parkinson's disease (AD and PD) and that includes the highly controversial approval of the Aβ-targeting antibody aducanumab for the treatment of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the human tau gene cause frontotemporal dementia and Parkinsonism associated with chromosome 17 (FTDP-17). 3 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that immunostaining with these antibodies is essential for the evaluation of frontal dementia. 2 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
RNA therapeutics comprise a diverse group of oligonucleotide-based drugs such as antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), and short hairpin RNAs (shRNAs) that can be designed to selectively interact with drug targets currently undruggable with small molecule-based drugs or monoclonal antibodies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathological findings of corticobasal degeneration are associated with several distinct clinical syndromes, and the corticobasal syndrome has been linked with a number of diverse pathologies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aging population worldwide is facing a significant increase in age-related non-communicable diseases, including cardiovascular and brain pathologies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Studies in neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Amyotrophic lateral sclerosis, Huntington's disease, and so on, have suggested that inflammation is not only a result of neurodegeneration but also a crucial player in this process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress has been linked with a variety of diseases, being involved in the debut and/or progress of several neurodegenerative disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders are primarily characterized by neuron loss. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
α-Synuclein aggregation is implicated in a variety of diseases including Parkinson's disease, dementia with Lewy bodies, pure autonomic failure and multiple system atrophy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synucleinopathies, which include multiple system atrophy (MSA), Parkinson's disease, Parkinson's disease with dementia and dementia with Lewy bodies (DLB), are human neurodegenerative diseases 1 . 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,696 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 29,380 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 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →