Late-life dementia has a strong heritable component. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Late-life dementia has a strong heritable component. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
= 0.022). Our approach captured the complex morphological alterations of the ChP in AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In a family with autopsy-confirmed Alzheimer disease, the authors found a mutation in the presenilin 2 (PS2) gene (PSEN2) that predicts a methionine-to-isoleucine change at PS2 residue 239 (M239I), at which a change to valine was known in another family. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The mean AAO was 46.9 years (median 45 years; range 33 to 60 years). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuropathologic examination revealed Alzheimer-type changes with Abeta in neuritic plaques and vessel walls, but the cognitive profile of the patients differed from that in AD, as the visuoconstructive functions and verbal fluency were well preserved even in the moderate stage of the disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The CAA and HTN-ICH groups had similar age (66.9 vs 67.1), sex, and leukoaraiosis volumes (31 vs 30 mL, all p > 0.8). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Five patients developed a stereotyped syndrome of progressive akinesia of gait, speech, and hand-writing without rigidity, tremor, or dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The extent and location of neuronal losses necessary or sufficient to produce dementia in patients with Alzheimer's Disease (AD) is unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic dysfunction and failure are processes that occur early in Alzheimer disease (AD) and are important targets for protective treatments to slow AD progression and preserve cognitive and functional abilities. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study supports previous findings of heterogenous pathology in essential tremor (ET). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a high incidence on Guam of a severe tauopathy known as the Parkinson- dementia complex (PDC). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From a series of 460 dementia patients referred to a regional brain bank, 14 (3%) patients had a pathologic diagnosis of primary degeneration of the brain involving multiple sites (frontoparietal cortex, striatum, medial thalamus, substantia nigra, and hypoglossal nucleus), with cell loss and astrocytosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Patients with neurologic or general conditions associated with an increased risk of falling should be asked about recent falls and further examined for the presence of specific neurologic deficits that predict falls, which include gait and balance disorders; deficits of lower extremity strength, sensation, and coordination; and cognitive impairments. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We designed this questionnaire-based study to determine the risk of auto crashes among Alzheimer's disease (AD) patients who continued to drive after the onset of AD, compared with normal age-matched control subjects and other drivers' statistical records. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research suggests that Alzheimer disease (AD) pathophysiology begins prior to the clinical expression of the disease and that biomarker measures may provide direct evidence of this process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors identified 2 Class I studies, 8 Class II studies, and 30 Class III studies in ALS, but many important areas have been little studied. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both the amygdala and the hippocampus are involved in the pathogenesis of a number of neurologic conditions, including temporal lobe epilepsy, postanoxic amnesia, and Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a reduction in the volume of amygdala and hippocampus in people with autism, particularly in relation to total brain volume. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We investigated the relationship between preoperative MRI hippocampal volumes and clinical neuropsychological memory test data obtained before and after temporal lobectomy and amygdalohippocampectomy for intractable epilepsy in 44 left (LTL) and 36 right (RTL) temporal lobectomy patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The objective of this study was to use high-resolution MRI techniques to determine whether children with Down syndrome exhibit decreases in hippocampal and amygdala volumes similar to those demonstrated in recent studies of adults with this condition. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We examined the relation of APOE-epsilon 4, hippocampal volume, and cognitive performance in ten pairs of cognitively normal twins who had a mean age of 62.5 years (SD = 7.8). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Data on behavioral changes after thalamic lesion are sparse and largely based on isolated reports of patients with thalamic strokes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data suggest that low-grade inflammation as assessed by high-sensitivity C-reactive protein is associated with cerebral microstructural disintegration that predominantly affects frontal pathways and corresponding executive function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The spectrum of mutations in this study can be used to plan appropriate screening protocols; a suggested protocol is to screen exon 4, and proceed to exons 3, 5, and 6 where indicated. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Screening tools are available for depression and dementia in patients with PD, but more specific validated tools are needed. 1 key finding →
Evidence: low
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 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 →