30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
We showed that consumer wearables are a valid tool for long-term data collection in this vulnerable patient population. 3 key findings →
Participants: 16 Evidence: low
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Utilizing machine learning, we identify a 12-protein panel from cerebrospinal fluid proteomic datasets. 5 key findings →
Evidence: low
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Oculomics is an emerging field that leverages ophthalmic imaging data to identify biomarkers of systemic disease, facilitating early diagnosis and risk stratification. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Diabetic-related cognitive dysfunction, especially mild cognitive impairment (MCI), is a serious complication of type 2 diabetes mellitus (T2DM). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
While the β-secretase BACE1 is responsible for the rate-limiting initial step to generate amyloid-β (Aβ) peptides, BACE1 inhibitor clinical trials have been halted due to a lack of efficacy and/or safety concerns at symptomatic/prodromal stages of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Gene-proxy for Graves' disease was associated with an increased risk of major depressive disorder (P-value = 0.02), whereas gene-proxy for autoimmune thyroiditis was linked to a greater risk of bipolar disorder (P-value = 0.043). 4 key findings →
Evidence: low
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
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Understanding the distribution of SV2A in DS will provide insight on changes to synaptic density in populations with accelerated AD neuropathology. 3 key findings →
Participants: 94 Evidence: moderate
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Accurate classification of neurodegenerative disorders remains a challenge in neuroscience. 3 key findings →
Evidence: low
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Existing models of frontotemporal dementia (FTD) may not fully recapitulate the pathophysiology of the disease. 1 key finding →
Evidence: low
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Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →
Evidence: low
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Lewy bodies and neurofibrillary tangles, composed of α-synuclein (α-syn) and tau, respectively, often are found together in the same brain and correlate with worsening cognition. 3 key findings →
Evidence: low
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Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →
Evidence: low
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Tau mutant cortical organoids showed altered mitochondrial function and gene expression related to neuronal development, with synaptic markers and neuronal activity reduction. 5 key findings →
Evidence: low
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In addition to the core clinical features of fluctuating cognition, visual hallucinations, and parkinsonism, individuals with dementia with Lewy bodies (DLB) frequently experience chronic and debilitating major depression. 2 key findings →
Evidence: low
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= 62.87, SD = 9.46, 36.52% female). Both networks were densely connected, reflecting comorbidity between neuropsychiatric symptoms and cognitive scores. 5 key findings →
Evidence: low
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Mild Cognitive Impairment (MCI) is a transitional stage between normal age-related cognitive decline and the more severe cognitive loss seen in dementia. 1 key finding →
Evidence: low
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At baseline, the mean ZBI score was 24.5 ± 15.2 and correlated positively with caregiver CES-D and STAI scores and with patient neuropsychiatric symptoms (NPI-frequency × severity) and distress felt by the caregiver (NPI-distress). 4 key findings →
Evidence: low
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Mild cognitive impairment (MCI) and sarcopenia are prevalent age-related conditions that often coexist and share common mechanisms such as chronic inflammation, reduced neuroplasticity, and impaired muscle function. 1 key finding →
Design: narrative review Evidence: low
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The results of the data analysis revealed two main categories: emotional schemas in mild cognitive impairment and understanding the meaning of the diagnosis. 5 key findings →
Participants: 16 Evidence: low
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The rising global prevalence of Alzheimer's disease (AD) and mild cognitive impairment (MCI) underscores the urgent need to elucidate their underlying pathogenic mechanisms. 4 key findings →
Evidence: low
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Our findings showed the strong predictive potential of PET, particularly florbetaben (FBB), which achieved an AUC of 0.84. 5 key findings →
Participants: 487 Evidence: low
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Overall, both machine learning techniques had an equivalent performance. 4 key findings →
Evidence: low
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These findings highlight hippocampal atrophy as a key pathway linking Aβ burden to cognitive impairment. 4 key findings →
Evidence: moderate
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Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease without effective treatments. 1 Extracellular amyloid plaques, neurofibrillary tangles, neuroinflammation, and neuronal loss are the characteristics of AD neuropathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 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