31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Microglia are implicated in the progression of Alzheimer's disease (AD) pathology from its earliest stages, suggesting that cerebrospinal fluid (CSF) microglia profiling across clinical AD stages can aid in treatment development and monitoring. 3 key findings →
Participants: 834 Evidence: low
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Early and accurate detection of Alzheimer's disease (AD) is essential for timely intervention and development of disease-modifying treatments. 1 key finding →
Design: longitudinal study Evidence: moderate
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Among the more than 90 identified genetic risk loci for late-onset Alzheimer's disease (AD) and related dementias, the apolipoprotein E (APOE) gene ɛ2/ɛ3/ɛ4 polymorphisms remain the longstanding benchmark for genetic disease risk with a consistently large effect across studies 1-10 . 5 key findings →
Design: case-control Evidence: high
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Better cognitive outcome and higher synaptic density in PS2APP mice was predicted by higher TSPO expression at 8 mo. The progression of TSPO activation to 13 mo also showed a moderate association with spared cognition, but amyloidosis did not correlate with the cognitive outcome, regardless of the time point. 3 key findings →
Design: longitudinal study Evidence: moderate
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Brain Aβ deposition is a key early event in the pathogenesis of Alzheimer´s disease (AD), but the long presymptomatic phase and poor correlation between Aβ deposition and clinical symptoms remain puzzling. 5 key findings →
Evidence: low
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Positron emission tomography (PET) with 18 F-fluorodeoxyglucose (FDG) reveals altered cerebral metabolism in individuals with mild cognitive impairment (MCI) and Alzheimer's dementia (AD). 4 key findings →
Participants: 332 Evidence: low
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Isolated rapid eye movement sleep behavior disorder (iRBD) is a major prodromal marker of α-synucleinopathies, often preceding the clinical onset of Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy. 3 key findings →
Participants: 31 Evidence: moderate
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Frontotemporal dementia, a heterogeneous neurodegenerative disorder, is a common cause of young onset dementia (i.e. dementia developing in midlife or earlier). 5 key findings →
Evidence: low
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The 2024 Lancet Commission Report on dementia prevention has identified 14 modifiable risk factors that account for approximately 45% of global dementia cases. 2 key findings →
Evidence: low
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In Alzheimer's disease (AD), a single-nucleotide polymorphism in the gene encoding brain-derived neurotrophic factor (BDNF Val66Met ) is associated with worse impact of primary AD pathology (beta-amyloid, Aβ) on neurodegeneration and cognitive decline, rendering BDNF Val66Met an important modulating factor of cognitive impairment in AD. 5 key findings →
Participants: 149 Evidence: low
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Brain atrophy occurs in aging even in the absence of dementia, but it is unclear to what extent this is due to undetected preclinical Alzheimer disease. 2 key findings →
Design: cross-sectional Evidence: moderate
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Amyloid imaging with PET and measuring cortical thickness with MRI are suitable biomarkers to detect disease progression in early AD within a small sample. 3 key findings →
Design: longitudinal study Evidence: moderate
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Pseudotemporal measurements from baseline PET data explained 87% ( P Pseudotemporal analysis of baseline PET images is capable of predicting the regional pattern of longitudinal Aβ accumulation in AD at a group level. 3 key findings →
Design: longitudinal study Participants: 58 Evidence: moderate
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The intramembrane protease γ-secretase is a hetero-tetrameric protein complex with presenilin as the catalytic subunit and cleaves its membrane protein substrates within their single transmembrane domains. γ-Secretase is well known for its role in Notch signalling and in Alzheimer's disease, where it catalyzes the formation of the pathogenic amyloid β (Aβ) peptide. 4 key findings →
Evidence: low
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Autosomal dominant cerebellar ataxia, deafness and narcolepsy (ADCA-DN) is characterized by late onset (30-40 years old) cerebellar ataxia, sensory neuronal deafness, narcolepsy-cataplexy and dementia. 4 key findings →
Evidence: low
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Our findings suggest that non-economic social deprivation, especially in terms of access to a grocery store, pharmacy, postal office, and bus stop, might be relevant for maintaining cognitive functioning in old age. 4 key findings →
Design: longitudinal study Participants: 91 Evidence: moderate
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Our findings support speech-based cognitive assessments as a promising avenue towards remote MCI screening, with implications for scalable screening in clinical trials and healthcare. 3 key findings →
Participants: 110 Evidence: low
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Patients with dementia face increased risks after general anesthesia. 4 key findings →
Participants: 27 Evidence: low
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Elevated microglial activation in the right amygdala-entorhinal-hippocampal complex of App NL-G-F mice is associated with better spatial learning. 5 key findings →
Design: cross-sectional Evidence: low
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Among 124 876 cases and controls, genome-wide conjunction analyses of ALS, FTD, PD, AD, CBD, and PSP revealed significant genetic overlap between ALS and FTD at known ALS loci: rs13302855 and rs3849942 (nearest gene, C9orf72; P = .03 for rs13302855 and P = .005 for rs3849942) and rs4239633 (nearest gene, UNC13A; P = .03). 3 key findings →
Evidence: low
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Keeping these concentrations below the tolerance values prevents the development of manifest and subclinical signs of aluminum toxicity. 2 key findings →
Evidence: low
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Increased peripheral and central nervous system cortisol levels have been reported in Alzheimer's disease (AD) and may reflect dysfunction of cerebral components of the hypothalamic-pituitary-adrenal (HPA) axis. 4 key findings →
Evidence: low
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Proregenerative responses are required for the restoration of nervous-system functionality in demyelinating diseases such as multiple sclerosis (MS). 4 key findings →
Evidence: low
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The clusters of significant depression and compensation were further used as volumetric regions of interest (ROIs) in a brain interregional correlation analysis in each prodromal AD subgroup to explore metabolic connectivity. 3 key findings →
Evidence: low
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Higher scores in cognitive screening [odds ratio (OR): 1.23], facial emotion processing (OR: 1.69), episodic memory (OR: 1.09), animal fluency (OR: 1.17), working memory (OR: 1.18), letter fluency (OR: 1.17) and depressive symptoms (OR: 7.41) were significantly associated with PPD (all Ps ≤ 0.010). 2 key findings →
Evidence: low
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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.
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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