28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Patients with Parkinson disease (PD) can experience hallucinations (spontaneous aberrant perceptions) and illusions (misinterpretations of real perceptual stimuli). 5 key findings →
Design: cross-sectional Evidence: low
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In 1975, tau protein was isolated as a microtubule-associated factor from the porcine brain. 5 key findings →
Evidence: low
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In 2006, TAR DNA-binding protein 43 (TDP-43), a highly conserved nuclear protein, was identified as the major disease protein in amyotrophic lateral sclerosis (ALS) and in the most common variant of frontotemporal lobar degeneration (FTLD), FTLD-U, which is characterized by cytoplasmic inclusions that stain positive for ubiquitin but negative for tau and alpha-synuclein. 5 key findings →
Evidence: low
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The neurodegenerative diseases are a diverse group of disorders characterized by progressive loss of specific groups of neurons. 5 key findings →
Evidence: low
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Frontotemporal dementia (FTD) refers to a group of progressive neurodegenerative disorders with different pathological signatures, genetic variability and complex disease mechanisms, for which no effective treatments exist. 4 key findings →
Evidence: low
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Age-related hearing impairment (ARHI, also known as presbycusis) is potentially a reversible risk factor for dementia and Alzheimer disease (AD). 2 key findings →
Evidence: high
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Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). 1 key finding →
Evidence: low
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Microglia are resident macrophages of the CNS that are involved in its development, homeostasis and response to infection and damage. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Drug repositioning and repurposing can enhance traditional drug development efforts and could accelerate the identification of new treatments for individuals with Alzheimer disease (AD) dementia and mild cognitive impairment. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Primary progressive aphasia (PPA) is a disorder of declining language that is a frequent presentation of neurodegenerative diseases such as frontotemporal lobar degeneration. 2 key findings →
Evidence: low
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Diffuse axonal injury after traumatic brain injury (TBI) produces neurological impairment by disconnecting brain networks. 5 key findings →
Evidence: low
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Since the original description of amyloid-β plaques and tau tangles more than 100 years ago, these lesions have been considered the neuropathological hallmarks of Alzheimer disease (AD). 1 key finding →
Evidence: low
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Classic textbook neurology teaches that amyotrophic lateral sclerosis (ALS) is a degenerative disease that selectively affects upper and lower motor neurons and is fatal 3-5 years after onset--a description which suggests that the clinical presentation of ALS is very homogenous. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
On 7 June 2021, aducanumab was granted accelerated approval for the treatment of Alzheimer disease (AD) by the FDA on the basis of amyloid-lowering effects considered reasonably likely to confer clinical benefit. 4 key findings →
Evidence: low
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Individuals over 80 years of age represent the most rapidly growing segment of the population, and late-life dementia has become a major public health concern worldwide. 4 key findings →
Evidence: low
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Incident stroke has long been recognized to cause dementia shortly after the event. 3 key findings →
Evidence: low
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Neurological illnesses, including cognitive impairment, memory decline and dementia, affect over 50 million people worldwide, imposing a substantial burden on individuals and society. 2 key findings →
Evidence: low
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Researchers have begun to characterize the subtle biological and cognitive processes that precede the clinical onset of Alzheimer disease (AD), and to set the stage for accelerated evaluation of experimental treatments to delay the onset, reduce the risk of, or completely prevent clinical decline. 4 key findings →
Evidence: low
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Despite tremendous investments in understanding the complex molecular mechanisms underlying Alzheimer disease (AD), recent clinical trials have failed to show efficacy. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia (FTD) refers to a group of clinically and genetically heterogeneous neurodegenerative disorders that are a common cause of adult-onset behavioural and cognitive impairment. 4 key findings →
Evidence: low
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Over the past decade, public awareness of the long-term pathological consequences of traumatic brain injury (TBI) has increased. 4 key findings →
Evidence: low
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Alzheimer disease (AD) is one of the most prevalent chronic medical conditions affecting the elderly population. 2 key findings →
Evidence: low
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Pure vascular parkinsonism without evidence of nigral Lewy body pathology may occur as a distinct clinicopathological entity, but a much more frequent occurrence is the comorbid presence of age-associated white matter lesions (WMLs) in idiopathic Parkinson disease (PD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prevention of Alzheimer disease (AD) is a medical challenge owing to its complex pathogenesis, which involves amyloid-β (Aβ) and tau aggregation, neuroinflammation and progressive neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent high-profile failures of Alzheimer disease treatments at the clinical trial stage have led to renewed efforts to identify and test novel interventions for Alzheimer disease and related dementias (ADRD). 5 key findings →
Evidence: high
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. 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 →