Bundles of paired helical filaments (PHF) accumulate in the pyramidal neurons that degenerate during Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
29,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tau immunoreactivity was studied in temporal neocortex, area 22, in 15 cases with graded intellectual status and compared with the immunoreactivity observed with an antiserum against paired helical filaments (PHF) and with the density of amyloid revealed by thioflavin S. Samples came from women over 75 years either intellectually normal or affected by senile dementia of the Alzheimer type at various degrees of severity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and neuropsychological studies of chronically institutionalized patients with schizophrenia indicate that severe cognitive impairment and functional disability in late life are very prevalent. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Argyrophilic grain disease (AgD), a frequent type of late onset dementia, is characterized by the occurrence of Gallyas-stained neuropil grains in the hippocampus, entorhinal cortex, amygdala and hypothalamus. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The nucleus basalis of Meynert, the major source of cholinergic innervation of the cerebral cortex, was morphometrically investigated in 58 cases of neuropsychiatric disorders and compared to 14 controls. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In all dementing illnesses, increased microvascular pathology was evident compared to normal controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dementia is a frequent complication of Parkinson's disease (PD) and usually occurs late in the protracted course of the illness. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intercellular adhesion molecule-1 (ICAM-1) was localized immunohistochemically in postmortem brain tissue of Alzheimer's disease (AD), progressive supranuclear palsy, amyotrophic lateral sclerosis, Pick's disease, and controls. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The deposition of the amyloid beta-protein (Abeta) is a pathological hallmark of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monoamine oxidase (MAO) histochemistry has been performed in brains from patients with dementia of Alzheimer type (DAT) and aged controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two types of Alzheimer neurofibrillary tangles may be found in the hippocampus in senile dementia of the Alzheimer type. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau-immunoreactive astrocytes in progressive supranuclear palsy (PSP) have a distinctive morphology and are referred to as tufted astrocytes (TA). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of white matter lesions, which are frequently found in ischemic cerebrovascular disease and Alzheimer's disease, remains unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Both protein kinases and phosphoprotein phosphatases are important components of signal transduction systems in cells. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choroid plexus is an epithelial-endothelial vascular convolute within the ventricular system of the vertebrate brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic loss is the major neurobiological substrate of cognitive dysfunction in Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A 53-year-old Japanese woman with a point mutation in mitochondrial DNA (tRNALeu(UUR), nt3243) consistent with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and Alzheimer-type brain pathology is reported. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
To investigate the roles imposed on astrocytes for glutamate metabolism, a specific inhibitor of glutamine synthetase (GS), methionine sulfoximine (MSO), was repeatedly administered to rats and histopathological changes were correlated with glycogen accumulation and the immunocytochemistry of GS and glial fibrillary acidic protein (GFAP). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 29,380 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 29,380 records, built mostly from automated pulls of Europe PMC (63.3% of the library) and OpenAlex (17.3%), 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.
1,037 records (3.5% of the library) are not peer-reviewed — 964 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 →