27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Protein conformational diseases, including Alzheimer's, Huntington's, and Parkinson's diseases, result from protein misfolding, giving a distinct fibrillar feature termed amyloid. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid beta-peptide (Abeta)(1-42) oligomers have recently been discussed as intermediate toxic species in Alzheimer's disease (AD) pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid-beta (Abeta) into senile plaques in Alzheimer's disease (AD) is a hallmark neuropathological feature of the disorder, which likely contributes to alterations in neuronal structure and function. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A transmembrane aspartyl protease termed beta-site APP cleavage enzyme 1 (BACE1) that cleaves the amyloid-beta precursor protein (APP), which is abundant in neurons, is required for the generation of amyloid-beta (Abeta) peptides implicated in the pathogenesis of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Proteins can become modified by a large number of reactions involving reactive oxygen species. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by enhanced beta-amyloid peptide (betaA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An analysis of interaction terms in the Cox regression model found that those individuals who utilized in-home help services earlier in their dementia caregiving careers were more likely to delay institutionalization. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The two major neurodegenerative diseases Alzheimer's disease (AD) and Parkinson's disease (PD) are characterised by low levels in the brain of the neurotransmitters acetylcholine (ACh) and dopamine (DA), respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although physicians, nurses and relatives are all guided by the best interest of the patient, it seems that differences in religious beliefs, perspective of the patient, and responsibility can lead to different attitudes towards end-of-life decisions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The use of turmeric, derived from the root of the plant Curcuma longa, for treatment of different inflammatory diseases has been described in Ayurveda and in traditional Chinese medicine for thousands of years. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD) is a progressive disease that usually affects the motor system but is also associated with a non-motor symptom (NMS) complex that ranges from dribbling saliva, constipation, depression, sleep disorders, apathy, hallucinations, and dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study explores whether nursing home residents with Alzheimer's disease and related dementias (ADRD) are affected differently by facility-level risk factors of ambulatory care-sensitive (ACS) conditions, a measure of timely access to medical care. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
INPH can be diagnosed accurately with CSF pressure monitoring and CSF drainage via a spinal catheter. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Endocytosis is universally important in cell function. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulation of amyloid beta-protein (Abeta) is a fundamental feature of certain human brain disorders such as Alzheimer's disease (AD) and Down syndrome and also of the skeletal muscle disorder inclusion body myositis (IBM). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A progressive chain of pathophysiological events links cardiovascular risk factors to clinical manifestations of disease and life-threatening cardiovascular events. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The age-adjusted death rate for the United States decreased from 845.3 deaths per 100,000 population in 2002 to 831.2 deaths per 100,000 population in 2003. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering members of the DR family by death ligands results in the transduction of either apoptotic or survival signals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In 2002, the 10 leading causes of death were (in rank order) Diseases of heart; Malignant neoplasms; Cerebrovascular diseases; Chronic lower respiratory diseases; Accidents (unintentional injuries); Diabetes mellitus; Influenza and pneumonia; Alzheimer's disease; Nephritis, nephrotic syndrome and nephrosis; and Septicemia and accounted for about 79 percent of all deaths occurring in the United States. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) and Down syndrome (DS) brains contain deposits of amyloid-beta peptide that are located extracellularly in the neuropil and in blood vessels walls. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
It is well recognized that the number of older adults who suffer from dementia has been increasing and will continue to do so over the coming years. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Down syndrome (DS) patients suffer from mental retardation, but also display enhanced beta-APP production and develop cortical amyloid plaques at an early age. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Hyperphosphorylated microtubule-associated protein tau is the major protein component of neurofibrillary tangles in the brain of patients with Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Kaufman, “dying people are not wanted in medical institutions, and it shows.” 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal dementia regards a group of presenile progressive neurodegenerative form of dementias which includes Pick's disease, corticobasal degeneration, frontotemporal dementia with motor neuron disease, frontal lobe degeneration, dementia-parkinsonism-amyotrophy complex, familial non-specific dementia mapping to chromosome 3, non-Alzheimer degenerative dementia lacking distinctive histological features as well as a number other infrequent syndromes with dementia and focal neurological signs. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →