30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP) (also known as a-synuclein) is a presynaptic terminal molecule that accumulates in the plaques of Alzheimer's disease. 3 key findings →
Evidence: low
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Combined neuropathological and neurochemical assessment of the nucleus of Meynert in senile dementia of Alzheimer type (SDAT) have demonstrated that the cholinergic biochemical activity, choline acetyltransferase, is more extensively reduced in the nucleus (over 90%) than the loss of putative cholinergic perikarya (35%). 3 key findings →
Evidence: low
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Neuroinflammation and overactivated microglia underlies the pathogenesis of Parkinson's disease (PD). 4 key findings →
Evidence: low
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Most patients with dementia with Lewy bodies (DLB) exhibit diffuse plaque-only pathology with rare neocortical neurofibrillary tangles (NFTs), as opposed to the widespread cortical neurofibrillary-tau involvement in Alzheimer disease (AD). 4 key findings →
Participants: 33 Evidence: low
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PET of β-Amyloid plaques (Aβ) using [ 18 F ] florbetaben ( [ 18 F ] FBB) and [ 18 F ] fluorodeoxyglucose ( [ 18 F ] FDG) increasingly aid clinicians in early diagnosis of dementia, including Alzheimer's disease (AD), frontotemporal disease, dementia with Lewy bodies, and vascular dementia. 4 key findings →
Participants: 40 Evidence: low
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Differences in regional cerebral blood flow (rCBF) between subjects with Alzheimer's disease (AD), dementia with Lewy bodies (DLB) and healthy volunteers were investigated using statistical parametric mapping (SPM99). 4 key findings →
Evidence: low
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Neuroinflammatory changes play a pivotal role in the progression of Parkinson's disease (PD) pathogenesis. 4 key findings →
Evidence: low
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Reactive microgliosis, hallmark of neuroinflammation, may contribute to neuronal degeneration, as shown in several neurodegenerative diseases. 4 key findings →
Evidence: low
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Vascular dementia (VD) is defined as a progressive neurodegenerative disease of cognitive decline, attributable to cerebrovascular factors. 4 key findings →
Evidence: low
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Living in more deprived neighborhoods was associated with an accelerated disease course in bvFTD, highlighting an important socioeconomic disparity in disease prognosis. 3 key findings →
Design: longitudinal study Participants: 161 Evidence: moderate
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Research interest in the application of electroencephalogram (EEG) as a non-invasive diagnostic tool for the automated detection of neurodegenerative diseases is growing. 2 key findings →
Participants: 88 Evidence: moderate
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We found that sleep disorders were associated with risk of Alzheimer’s disease (AD), amyotrophic lateral sclerosis, dementia, Parkinson’s disease (PD), and vascular dementia in three national biobanks (hazard ratios from 1.3 (PD) to 5.11 (dementia)). 2 key findings →
Evidence: low
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Vascular dementia (VaD) is a heterogeneous group of brain disorders caused by cerebrovascular pathologies and the second most common cause of dementia, accounting for over 20% of cases and posing an important global health concern. 5 key findings →
Evidence: low
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Cerebrolysin (CBL) is a combination of neurotrophic peptides and amino acids derived from pig brains. 1 key finding →
Evidence: low
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Mutations in the TARDBP gene encoding TDP-43 protein are linked to loss of function in neurons and familial frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). 5 key findings →
Evidence: low
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Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
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Surprisingly, levels of strain A and B aSyn species were higher in plasma from individuals with PD compared to DLB in 2 independent cohorts. 5 key findings →
Evidence: low
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Forty bvFTD patients and 40 HC (56.25% female, mean age of 63.55 years) were involved. 5 key findings →
Participants: 36 Evidence: low
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Co-existing neuropathology was frequent, even among individuals without clinical dementia. 5 key findings →
Evidence: moderate
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The majority of individuals at 50% risk of carrying a pathogenic variant causing frontotemporal dementia (FTD) chooses not to undergo presymptomatic genetic testing. 5 key findings →
Participants: 14 Evidence: low
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These findings establish IF as a potent modulator of synaptic resilience in VaD, acting through coordinated preservation of synaptic structure, inhibition of inflammatory synapse loss, and metabolic reprogramming. 2 key findings →
Evidence: low
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In DLB, plasma concentrations of GFAP and NfL were associated with MTA, GCA-F, and Fazekas scale; and the Aβ42/40 ratio was associated with PA and Fazekas. 5 key findings →
Participants: 92 Evidence: low
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Neuropsychiatric symptoms (NPS) are prevalent, emerge early, and are associated with poorer outcomes in Lewy body dementia (LBD). 5 key findings →
Participants: 28 Evidence: low
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Dopamine transporter (DAT) imaging and electroencephalography (EEG) are recommended biomarkers for diagnosing dementia with Lewy bodies (DLB). 4 key findings →
Participants: 120 Evidence: low
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The Benson Complex Figure Test (BCFT) is a neuropsychological tool designed to assess visuospatial construction and visual memory with lower complexity than traditional tests. 4 key findings →
Design: cross-sectional Participants: 1,428 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 2,748 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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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 →