28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Advanced age and presence of intracerebral amyloid deposits are known to be major risk factors for development of neurodegeneration in Alzheimer's disease (AD), and both have been associated with microglial activation. 4 key findings →
Evidence: low
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Alzheimer's disease is characterized by degenerative changes in a variety of neurotransmitter systems. 4 key findings →
Evidence: low
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Formalin-fixed postmortem brain tissue from 14 HIV-infected adult patients, with previous repeated neurological and neuroradiological examinations, was studied by immunohistochemical and molecular biological methods. 4 key findings →
Evidence: low
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Neuroinflammation is common to various diseases of the central nervous system (CNS), but its imprecise definition has led to many misconceptions in research and clinical approaches. 3 key findings →
Evidence: low
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Microglia are endogenous brain macrophages that show distinct phenotypes such as expression of myeloid antigens, ramified morphology, and presence within the neural parenchyma. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Activated astrocytes, overexpressing the neurotrophic signaling molecule S100beta, are invariant components of the Abeta plaques of Alzheimer's disease. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder primarily characterized by excessive deposition of amyloid-beta (Abeta) peptides in the brain. 4 key findings →
Evidence: low
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Traumatic brain injury (TBI) is a significant risk factor for chronic traumatic encephalopathy (CTE), Alzheimer's disease (AD), and Parkinson's disease (PD). 4 key findings →
Evidence: low
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Alzheimer's disease (AD) is the most common form of dementia among the elderly, characterized by amyloid plaques, neurofibrillary tangles, and neuroinflammation in the brain, as well as impaired cognitive behaviors. 4 key findings →
Evidence: low
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In most neurodegenerative disorders, including multiple sclerosis, Parkinson disease, and Alzheimer disease, a massive neuronal cell death occurs as a consequence of an uncontrolled inflammatory response, where activated astrocytes and microglia and their cytotoxic agents play a crucial pathological role. 4 key findings →
Evidence: low
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Greater TSPO is associated with lower performance in episodic memory, attention/processing speed, executive function, language, and visuospatial ability in amyloid-positive individuals, but restricted to episodic memory in amyloid-negative individuals. 2 key findings →
Design: cross-sectional Participants: 21 Evidence: low
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The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies. 5 key findings →
Evidence: low
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Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. 1 key finding →
Evidence: low
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Frontotemporal dementia is a debilitating neurodegenerative disorder characterized by frontal and temporal lobe degeneration, resulting in behavioral changes, language difficulties, and cognitive decline. 2 key findings →
Evidence: low
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AD patients exhibited increased expression of pyroptosis-related genes, supporting the involvement of pyroptosis in neurodegeneration. 5 key findings →
Evidence: low
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Whereas neurotoxic Aβ is derived from amyloid precursor protein (APP) by β- and γ-secretase cleavage, APP processing along the non-amyloidogenic pathway results in the secretion of the large neurotrophic ectodomain APPsα. 2 key findings →
Evidence: low
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Although the relationship between macroautophagy/autophagy and Alzheimer disease (AD) is widely studied, the underlying mechanisms are poorly understood, especially the regulatory role of the initiation signaling of autophagy on AD. 2 key findings →
Evidence: low
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Female Psen1 mutation(L166P) mice were found to have reductions in whole-body mineral density (BMD) and bone mineral content as early as one month and a sustained bone phenotype with age with loss in cortical and trabecular properties compared to age-and gendermatched wildtype control mice, whereas male mice did not (Fig.1A-C). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
TDP-43 is a ubiquitously expressed, primarily nuclear DNA/RNA-binding protein implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD). 1 key finding →
Evidence: low
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TDP-43 pathology is a hallmark of fatal neurodegenerative disorders, including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and limbic-predominant age-related TDP-43-encephalopathy (LATE). 1 key finding →
Evidence: low
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We show that TDP-43 activates GSK3 and promotes caspase-dependent cleavage of TDP-43, generating C-terminal fragments. 2 key findings →
Evidence: low
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The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), highlighted the virus's impact on the central nervous system and its potential to exacerbate neurodegenerative diseases, similar to that in Alzheimer disease (AD). 1 key finding →
Evidence: low
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Chronic cerebral hypoperfusion (CCH) is a major contributor to vascular dementia, with neuroinflammation playing a central role in its pathogenesis. 5 key findings →
Evidence: low
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Methylglyoxal (MG), a reactive dicarbonyl metabolite associated with diabetes and metabolic disorders, contributes to carbonyl stress, neuroinflammation, and Alzheimer-like neurodegeneration. 4 key findings →
Evidence: low
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Cerebral small vessel disease (cSVD) is a common cause of stroke and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
10 of the 6,970 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →