28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among the various disorders manifesting dementia, gait disturbance, and urinary incontinence in the elderly population, idiopathic normal pressure hydrocephalus (iNPH) is becoming of great importance. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The objective of this study was to assess the temporal relationship between changes in predominant motor symptoms and incident dementia in Parkinson's disease (PD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative disorder with core features of action tremor and cerebellar gait ataxia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gait impairment is a prominent falls risk factor and a prevalent feature among older adults with cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Functional decline in locomotion is common among the elderly, and the prevalence of gait disorders increases with age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia (FTD) is characterized by cognitive and behavioral changes and, in a significant subset of patients, Parkinsonism. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
INPH can be diagnosed accurately with CSF pressure monitoring and CSF drainage via a spinal catheter. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Besides cognitive decline, dementia is characterized by gait changes and increased fall risk, also in early stages of the disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the rapid aging of Japanese society, medical care of the elderly has become an important social issue. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twentieth-century hypotheses attributing a substantive role to aging in Parkinson disease (PD) pathogenesis have been countered by evidence from clinical, pathological, and biochemical investigations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This chapter reviews the neurological phenotype of Down syndrome (DS) in early development, childhood, and aging. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Thirty-one patients with Wilson's disease were evaluated with detailed neurologic and medical examinations. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The focus of this review is on the close relationship between gait and cognition in ageing and associated dementias. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease is the second most common neurodegenerative disease, after Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aggregation of alpha-synuclein, an abundant and conserved pre-synaptic brain protein, is implicated as a critical factor in several neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Nitric oxide (NO) and carbon monoxide (CO) synthesized from L-arginine by NO synthase and from heme by heme oxygenase, respectively, are the well-known neurotransmitters and are also involved in the regulation of vascular tone. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome is one of the major causes of mental retardation and congenital heart malformations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings link altered processing of beta-amyloid precursor protein (beta APP) to disruption of neuronal Ca2+ homeostasis and an excitotoxic mechanism of cell death in Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hydrogen sulfide is one of three gases involved in biological functions and synthesized in vivo. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Endocytosis is universally important in cell function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence points to an important role of intraneuronal A beta as a trigger of the pathological cascade of events leading to neurodegeneration and eventually to Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and change in personality. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An additional copy of the beta-amyloid precursor protein (APP) gene causes early-onset Alzheimer's disease (AD) in trisomy 21 (DS). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Individuals with Down syndrome (DS) commonly possess unique neurocognitive and neurobehavioral profiles that emerge within specific developmental periods. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid beta-protein (Abeta) is a fundamental feature of certain human brain disorders such as Alzheimer's disease (AD) and Down syndrome and also of the skeletal muscle disorder inclusion body myositis (IBM). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Human cellular models of Alzheimer's disease (AD) pathogenesis would enable the investigation of candidate pathogenic mechanisms in AD and the testing and developing of new therapeutic strategies. 1 key finding →
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →