Alterations in synaptic protein stoichiometry may contribute to neocortical synaptic dysfunction in Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alterations in synaptic protein stoichiometry may contribute to neocortical synaptic dysfunction in Alzheimer disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The purpose of this article is to present a selective and concise summary of fluorodeoxyglucose (FDG) positron emission tomography (PET) in dementia imaging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive, neurodegenerative disorder and the most prevalent senile dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Regular physical activity undoubtedly has many health benefits for all age groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a pressing demand for improving the quality and efficacy of health care and social support services needed by the world's growing elderly population, especially by those affected by mild cognitive impairment (MCI) and Alzheimer's disease (AD)-type early-stage dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a critical need to potentially individualize new strategies able to prevent and to slow down the progression of predementia and dementia syndromes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The use of positive modulators of PLA2 (especially of cPLA2 and iPLA2) or supplementation with dietary lipid compounds (e.g., arachidonic acid) in combination with cognitive training could be a valuable therapeutic strategy for cognitive enhancement in early-stage AD. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Non-pharmacological interventions have the potential to reduce cognitive decline and to improve psychosocial aspects in mild cognitive impairment and Alzheimer's dementia, and the absence of side effects makes them a favorable option also for preventive strategies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The purpose of this article is to critically review and synthesize the literature on the effects of nonpharmacological cognitive training on dementia symptoms in early-stage Alzheimer's disease (AD) and related dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mild cognitive impairment (MCI) stage of dementia with Lewy bodies (MCI-DLB) has not yet been defined, but is likely to differ in the MCI stage of Alzheimer's disease (MCI-AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Efforts to clinically diagnose cases having dementia with Lewy bodies (DLB) identify those with a characteristic clinical syndrome (probable DLB) at the expense of missing an equal, if not greater, number of cases who have atypical presentations thought to be associated with coexisting Alzheimer pathologies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The patterns of subfield atrophy in AD and MCI were consistent with patterns of neuronal cell loss/reduced synaptic density described by histopathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The concept of amnestic mild cognitive impairment (MCI) describes older people who show a decline predominantly in memory function, but who do not meet criteria for dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The FDG-positive subgroup showed only hypometabolism, predominantly in AD-sensitive areas extending to the whole neocortex, compared with the FDG-negative subgroup. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
N-methyl-D-aspartate (NMDA) receptor antagonists have therapeutic potential in numerous CNS disorders ranging from acute neurodegeneration (e.g. stroke and trauma), chronic neurodegeneration (e.g. Parkinson's disease, Alzheimer's disease, Huntington's disease, ALS) to symptomatic treatment (e.g. epilepsy, Parkinson's disease, drug dependence, depression, anxiety and chronic pain). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results imply that individuals with MCI have increased brain oxidative damage before the onset of symptomatic dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Magnetic resonance imaging (MRI) patterns were examined together with cerebrospinal fluid (CSF) biomarkers in serial scans of Alzheimer's Disease Neuroimaging Initiative (ADNI) participants with mild cognitive impairment (MCI). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Oxidative stress has been implicated to play a crucial role in the pathogenesis of a number of diseases, including neurodegenerative disorders, cancer, and ischemia, just to name a few. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A PET tracer is desired to help guide the discovery and development of disease-modifying therapeutics for neurodegenerative diseases characterized by neurofibrillary tangles (NFTs), the predominant tau pathology in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence suggests that subjective cognitive complaints (SCC) may indicate subtle cognitive decline characteristic of individuals with preclinical Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Arterial spin-labeling MR imaging showed regional hypoperfusion with AD, in brain regions similar to those seen in FDG PET and HMPAO SPECT studies of similar populations; this hypoperfusion persists after accounting for underlying cortical gray matter atrophy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There has been a dramatic increase in the number of studies using resting state functional magnetic resonance imaging (rs-fMRI), a recent addition to imaging analysis techniques. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Many machine learning and pattern classification methods have been applied to the diagnosis of Alzheimer's disease (AD) and its prodromal stage, i.e., mild cognitive impairment (MCI). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), brain lesions are marked by severe neuronal loss and retinal degeneration was previously mentioned in affected patients. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
PIB-PET imaging is a sensitive and specific marker for underlying Aβ amyloid deposition and represents an important investigative tool for examining the relationship between amyloid burden, clinical symptoms and structural and functional changes in dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
10 of the 2,090 studies in this tag, 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →