30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
It is widely known that exogenous formaldehyde exposure induces human cognitive impairment and animal memory loss; and recent studies show that formaldehyde at pathological levels induces Aβ deposition and misfolding of tau protein to form globular amyloid-like aggregates. 4 key findings →
Participants: 141 Evidence: low
Full summary, score breakdown and related studies → Original source
The first reports of disorders that in terms of cognitive and behavioral symptoms resemble frontotemporal dementia (FTD) and in terms of motor symptoms resemble amyotrophic lateral sclerosis (ALS) bring us back to the second half of the 1800s. Over the last 150 years, and especially in the last two decades, there has been growing evidence that FTD signs can be seen in patients primarily diagnosed with ALS, implying clinical overlap among these two disorders. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In 4 cases of Parkinson's disease (PD), 2 cases of Dementia with Lewy bodies (DLB) and 3 age-matched controls, the TUNEL/ISEL method was used to detect DNA fragmentation in substantia nigra locus coeruleus and cerebral cortex [method by Gold et al. In addition, immunohistochemistry was performed for an array of apoptosis-related proteins, i.e. the recently described apoptosis specific protein cJun/AP1 (ASP), the proto-oncogenes c-Jun, c-Jun AP1, Bcl2, Bax, Bcl-x, p53, CD 95 (Fas/Apo-1) 4 key findings →
Evidence: low
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Dementia is a growing problem of global relevance, currently affecting over 55 million people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia with Lewy bodies (DLB) is thought to be the second most common form of dementia after Alzheimer’s disease, and is characterised by a combination of cognitive, neuropsychiatric and motor symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The mean age of the 3 women and 18 men was 50 years (range, 26-68 years). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial frontotemporal dementia (fFTD) is an autosomal dominant heritable form of FTD, onsetting in mid-life, characterized by behavioral and personality changes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• Executive dysfunction is a key characteristic of bvFTD. • Network de-differentiation reflects loss of specialized networks. • De-differentiation of the salience network relates to executive dysfunction in bvFTD. • Reduced network capacity for specialized processing may mediate emergence of executive dysfunction. 5 key findings →
Participants: 90 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Our multi-omics study revealed distinct gut microbiota and metabolite alterations in PD patients with cognitive impairment, highlighting gut-brain axis dysfunction. 5 key findings →
Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 seeding activity was detected in 67% of TDP-43-linked symptomatic patients, with a specificity of 93%. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
86.8% of patients in this cohort presented more than one pathology. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) are the two most common forms of dementia due to neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Mediterranean diet, rich in plant-based foods, olive oil, and fish, has been consistently associated with slower cognitive decline and reduced risk of neurodegeneration in observational studies and some clinical trials. 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
This article describes pathogenic concepts and factors, in particular glycolipid abnormalities, that create cell dysfunction and synaptic loss in neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest that microglial activation and the production of proinflammatory mediators by phospho-tau-positive neurons and glial cells may differentially contribute to neuronal death and disease progression in neurodegenerative tauopathies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Various methods of rehabilitation for dysphagia have been suggested through the experience of treating stroke patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The fundamental role that alpha-synuclein (aSyn) plays in the pathogenesis of neurodegenerative synucleinopathies, including Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy, is a well-accepted fact. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Myeloperoxidase (MPO) is a key enzyme in inflammatory and degenerative processes, although conflicting reports have been presented concerning its expression in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathological investigations report that in synucleinopathies with dementia, namely Parkinson's disease (PD) with dementia (PDD) and dementia with Lewy bodies (DLB), the histopathological hallmarks of Alzheimer's Disease (AD), in particular amyloid plaques, are frequently observed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is the second most common neurodegenerative disorder after Alzheimer's disease, affecting approximately 1 percent of the population over age 50. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rapid eye movement sleep behavior disorder is characterized by dream enactment and complex motor behaviors during rapid eye movement sleep and rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia) during polysomnography. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD) is a clinically and pathologically heterogeneous syndrome, characterized by progressive decline in behaviour or language associated with degeneration of the frontal and anterior temporal lobes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Age, sex, functional and cognitive impairment and the diagnosis of pneumonia or congestive heart failure were the strongest predictors of death. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Determining the relative contributions of environment and heredity to the cause of Parkinson's disease (PD) is more than an academic issue because its resolution dictates future research directions to an enormous degree. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
This article reviews evidence for the occurrence of atypical parkinsonism in Afro-Caribbean and Indian ethnic minority subjects living in western countries, particularly the UK. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 1,072 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events