The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p > 0.8). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p > 0.8). 5 key findings →
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
Despite the rapidly ageing population and a predicted sevenfold increase in the prevalence of dementia in minority ethnic communities, people from these communities remain under-represented in specialist dementia services. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
SPLS outperformed PLS, finding statistically significant effects and providing higher correlation values in hold-out data. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common form of dementia, is a progressive disorder manifested by gradual memory loss and subsequent impairment in mental and behavioral functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Of the 8688 individuals in the Medicare Advantage population with a dementia diagnosis, 1061 (12.2%) received an antipsychotic medication. 4 key findings →
Participants: 8,688 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Acetylcholine (ACh) has a crucial role in the peripheral and central nervous systems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The incidence of dementia is higher in diabetic patients, but no effective treatment has been developed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed the prevalence of common altered brain proteins in 296 cognitively unimpaired subjects ranging from age 50 to 102 years. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that metformin pro-aggregation effects mitigate the potential benefits arising from its dephosphorylating action, possibly leading to an overall increase of the risk of tauopathy in elderly diabetic patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) and other tauopathies characterized by focal brain neurodegeneration and pathological accumulation of proteins are commonly associated with tau mutations. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
P021 is a small molecular weight, BBB permeable compound with suitable pharmacokinetics for oral administration, and without adverse effects associated with native CNTF or BDNF molecule. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hyperphosphorylated microtubule-associated protein tau is present in several neurodegenerative diseases, although the causal relationship remains elusive. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) has been associated with toxic intracellular aggregates of hyperphosphorylated tau (FTLD-tau). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mutations in the gene MAPT encoding tau, a microtubules-associated protein, cause a subtype of familial neurodegenerative disorder, known as frontotemporal lobar degeneration tauopathy (FTLD-Tau), which presents with dementia and is characterized by atrophy in the frontal and temporal lobes of the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is growing evidence of the involvement of advanced glycation end products (AGEs) in the pathogenesis of neurodegenerative processes including Alzheimer's disease (AD) and their function as a seed for the aggregation of Aβ, a hallmark feature of AD. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Virtual Reality (VR) has emerged as a promising tool in many domains of therapy and rehabilitation, and has recently attracted the attention of researchers and clinicians working with elderly people with MCI, Alzheimer's disease and related disorders. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive reserve (CR) is a potential mechanism to cope with brain damage. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive training offers the potential for individualised learning, prevention of cognitive decline, and rehabilitation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
At present there is a rapid growth of aging population groups worldwide, which brings about serious economic and social problems. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Physical and cognitive idleness constitute significant risk factors for the clinical manifestation of age-related neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It has been shown that cognitive training (CogTr) is effective and recuperative for older adults, and can be used to fight against cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
White matter deterioration in the aging human brain contributes to cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Causal treatments for neurodegenerative diseases are now being developed and tested, and thus a molecular diagnosis is desirable. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In view of its ability to explain the most frequent motor symptoms of Parkinson's Disease (PD), degeneration of dopaminergic neurons has been considered one of the disease's main pathophysiological features. 4 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 →