31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Vascular cognitive impairment is an umbrella term for cognitive dysfunction associated with and presumed to be caused by vascular brain damage. 2 key findings →
Participants: 10,515 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this in vivo study, we have demonstrated that microglial activation quantified using [ 11 C]PBR28 PET was associated with higher gray matter volume and higher hippocampal volume in patients with MCI. 4 key findings →
Design: longitudinal study Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Psychosis in Alzheimer's disease (AD) represents a distinct disease subtype with a more rapid progression of illness evidenced by an increased velocity of cognitive decline and a hastened mortality. 2 key findings →
Design: longitudinal study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In this cross-sectional study, abnormal central vascular hemodynamics were associated with higher tau burden in specific brain regions. 5 key findings →
Design: cross-sectional Participants: 3,171 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma tau is associated with cortical thickness and memory performance. 3 key findings →
Design: longitudinal study Participants: 378 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Our results provide further indirect support for the presumed link between superficial siderosis and cerebral amyloid angiopathy (CAA). 2 key findings →
Design: longitudinal study Participants: 1,062 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Both AD and TDP/HS contribute to hippocampal volume loss in older-old persons, with TDP/HS more strongly associated with hippocampal volume than AD in Alzheimer dementia. 3 key findings →
Design: cohort study Participants: 232 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Researchers used a tau PET agent to examine tau retention patterns in cognitively normal older people and compared them with young controls and Alzheimer's disease patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher amyloid beta burden was associated with increasing anxious-depressive symptoms over time in cognitively normal older individuals. 4 key findings →
Design: longitudinal study Participants: 270 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Patients with early-onset Alzheimer's disease (EOAD) are commonly excluded from large-scale observational and therapeutic studies due to their young age, atypical presentation, or absence of pathogenic mutations. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Post-mortem staging of Alzheimer's disease (AD) neurofibrillary pathology is commonly performed by immunohistochemistry using AT8 antibody for phosphorylated tau (p-tau) at positions 202/205. 3 key findings →
Participants: 47 Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF apoB markedly associates with early tau dysregulation in asymptomatic subjects and identifies at-risk individuals predisposed to develop visuospatial cognitive decline over time. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neurofibrillary tau tangles are a hallmark pathology of Alzheimer's disease (AD) and are more closely associated with AD-related cortical atrophy and symptom severity than amyloid-beta (Aβ). 5 key findings →
Design: longitudinal study Participants: 111 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The locus coeruleus (LC) is the brain's major source of the neuromodulator norepinephrine, and is also profoundly vulnerable to the development of Alzheimer's disease (AD)-related tau pathology. 3 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the brain accumulation of amyloid-β and tau proteins. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Studying autosomal dominant Alzheimer's disease (ADAD), caused by gene mutations yielding nearly complete penetrance and a distinct age of symptom onset, allows investigation of presymptomatic pathological processes that can identify a therapeutic window for disease-modifying therapies. 2 key findings →
Design: longitudinal study Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Does accelerated cortical atrophy in aging, especially in areas vulnerable to early Alzheimer's disease (AD), unequivocally signify neurodegenerative disease or can it be part of normal aging? 1 key finding →
Design: longitudinal study Participants: 1,100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
ARIA-E can also occur spontaneously in cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with increased CSF levels of anti-Aβ autoantibodies. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Interestingly, we found no consistent differences in learning and memory performance between high versus low PiB cognitively normal or amnestic MCI subjects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
β-Amyloid plaques and tau-containing neurofibrillary tangles are the two neuropathological hallmarks of Alzheimer's disease (AD) and are thought to play crucial roles in a neurodegenerative cascade leading to dementia. 2 key findings →
Design: longitudinal study Participants: 32 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The medial temporal lobe (MTL) is an early site of tau accumulation and MTL dysfunction may underlie episodic-memory decline in aging and dementia. 4 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Identifying high-risk populations is an important component of disease prevention strategies. 2 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent studies on Alzheimer's disease (AD) suggest that tau proteins spread through the brain following neuronal connections. 4 key findings →
Design: cross-sectional Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Assessment of medial temporal tau pathology will provide insights into early structural brain changes associated with later cognitive impairment and Alzheimer's disease. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 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