Neurons with lower basal UPS activity were more vulnerable to tau accumulation following mild UPS inhibition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The autophagy-lysosome pathway (ALP) and the ubiquitin-proteasome system (UPS) are the primary protein degradative mechanisms maintaining proteostasis in neurons. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
While amyloid precursor protein and the microtubule-associated protein tau demonstrated higher abundance in AD brains, no significant race-related differences were observed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This is primarily a mouse-model study (in amyloid-plaque mouse models such as 5xFAD, with some human tissue validation) identifying a newly recognized, protective state of brain immune cells (microglia) that expresses genes normally associated with the immune system's lymphocytes. 4 key findings →
Evidence: early
Full summary, score breakdown and related studies → Original source
Involvement of the immune system in the pathogenesis of Alzheimer's disease was demonstrated in two ways: by the attachment of complement proteins to diseased tissue, and by the activation of cells associated with the immune system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive neurodegenerative disorder, accompanied by memory loss and cognitive impairments, and there is no effective treatment for it at present. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Astrocytosis shows a distinct regional pattern in AD brain compared to fibrillar Aβ, suggesting that different types of astrocytes may be associated with the pathophysiological processes in AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Forty-one participants (30 male, 11 female) with a mean (SD) age at death of 75.7 (10.6) years were included. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Prevalent LB- and AD-related neurodegenerative pathologies affect a significant proportion of iNPH patients and contribute to cognitive decline (both) and motor impairment (only LB pathology) but do not significantly influence the surgical outcome at 6 months. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Aberrant cholesterol metabolism has been implicated in Alzheimer disease (AD) and other neurological disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
LR11 is an ApoE receptor that is enriched in the brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurofibrillary tangle predominant dementia (NFTPD) is a subset of late onset dementia, clinically different from traditional "plaque and tangle" Alzheimer disease (AD): later onset, shorter duration, less severe cognitive impairment, and almost absence of ApoE epsilon4. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
Neuropathological findings in three aged chimpanzees were compared with those in rhesus monkeys and individuals with Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
45/100
Both ATH and AD involve inflammation, macrophage infiltration, and occlusion of the vasculature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The low density lipoprotein receptor-related protein (LRP) is highly expressed in the brain and has been shown to alter the metabolism of amyloid precursor protein and amyloid-beta peptide (Abeta) in vitro. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The spatial relationship of apolipoprotein E (apoE)-like immunoreactivity (IR) to amyloid beta-peptide (A beta), astrocytes and microglial cells in the brain of Alzheimer's disease was studied by double immunolabelling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Stroke is a brain disease that occurs when blood flow stops, resulting in reduced oxygen supply to neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Global obesity is a pandemic status, estimated to affect over 2 billion people, that has resulted in an enormous strain on healthcare systems worldwide. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Apolipoprotein E (APOE) is a lipid-transport protein abundantly expressed in most neurons in the central nervous system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The association of neurofibrillary tangles with delayed verbal recall may reflect associated hippocampal atrophy. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The incidence of dementia is increasing at an alarming rate, and has become a major public health concern. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most common form of dementia, has increasing incidence, increasing mortality rates, and poses a huge burden on healthcare. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive memory loss and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Vascular dementia (VaD) is the second most common type of dementia after Alzheimer's disease (AD), characterized by progressive cognitive impairment, memory loss, and thinking or speech problems. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 6,970 studies in this tag that have a study page, 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.
- Tau Oligomer-Containing Synapse Elimination by Microglia and Astrocytes in Alzheimer Disease
- Type 2 diabetes, APOE gene, and the risk for dementia and related pathologies: The Honolulu-Asia Aging Study
- Very mild Alzheimer's disease: informant-based clinical, psychometric, and pathologic distinction from normal aging
- Plasma Aβ and neurofilament light chain are associated with cognitive and physical function decline in non-dementia older adults
- Distinct cytokine profiles in human brains resilient to Alzheimer's pathology
- TREM2 regulates microglial cell activation in response to demyelination in vivo
- Immunoreactivity of presenilin-1 in human, rat and mouse brain
- The DYRK1A gene, encoded in chromosome 21 Down syndrome critical region, bridges between beta-amyloid production and tau phosphorylation in Alzheimer disease
- Amyloid-beta aggregation implicates multiple pathways in Alzheimer's disease: Understanding the mechanisms
- The effects of chronic glucocorticoid exposure on dendritic length, synapse numbers and glial volume in animal models: implications for hippocampal volume reductions in depression
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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.
1,034 records (3.6% 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 →