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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 26–50 of 62 studies by Bennett DA · tagged Brain Biology (page 2 of 3) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 62 studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

Subjects

Other authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 16,851 studies have no institution on record and are not counted here.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

Characterization of mitochondrial DNA quantity and quality in the human aged and Alzheimer's disease brain

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Molecular neurodegeneration 2021-11-06

Changes in the mitochondrial DNA copy number (mtDNAcn) and increased mitochondrial DNA mutation burden have both been associated with neurodegenerative diseases and cognitive decline. 5 key findings →

Participants: 1,361 Evidence: low

Full summary, score breakdown and related studies → Original source

The relationship between cerebral Alzheimer's disease pathology and odour identification in old age

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Journal of neurology, neurosurgery, and psychiatry 2006-09-29

The results suggest that difficulty in identifying familiar odours in old age is partly due to the accumulation of neurofibrillar pathology in central olfactory regions. 2 key findings →

Participants: 166 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Multiple gene variants linked to Alzheimer's-type clinical dementia via GWAS are also associated with non-Alzheimer's neuropathologic entities

✓ Peer-reviewed alzhub usefulness score 56 out of 100. Neurobiology of disease 2022-09-30

The classic pathologic hallmarks of Alzheimer's disease (AD) are amyloid plaques and neurofibrillary tangles (AD neuropathologic changes, or ADNC). 4 key findings →

Participants: 273 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Neuropathologic Profiles and Associated Cognitive Trajectories in Community-Living Older Adults

✓ Peer-reviewed alzhub usefulness score 55 out of 100. JAMA Network Open 2026-01-02

Latent neuropathologic profiles were identified using hierarchical clustering, and longitudinal cognitive trajectories associated with each profile were estimated using functional mixed-effects models. 4 key findings →

Design: cohort Participants: 1,633 Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Stroke 2005-03-17

Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). 1 key finding →

Design: longitudinal study Participants: 96 Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Cerebral infarctions and the likelihood of dementia from Alzheimer disease pathology

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Neurology 2004-04-01

Cerebral infarctions independently contribute to the likelihood of dementia but do not interact with AD pathology to increase the likelihood of dementia beyond their additive effect. 2 key findings →

Participants: 153 Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Neuropathologic intermediate phenotypes enhance association to Alzheimer susceptibility alleles

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Neurology 2009-04-01

Discovery efforts for susceptibility loci for Alzheimer disease could benefit from the use of neuropathologic intermediate phenotypes as a complement to other approaches. 2 key findings →

Participants: 625 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Hippocampal sclerosis and TDP-43 pathology in aging and Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Annals of neurology 2015-04-22

Diagnoses of dementia, probable AD, and MCI in 636 autopsied subjects from the Religious Order Study and the Rush Memory and Aging Project were based on clinical evaluation and cognitive performance tests. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Diabetes is related to cerebral infarction but not to AD pathology in older persons

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2006-12-01

Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Epigenetic age of the pre-frontal cortex is associated with neuritic plaques, amyloid load, and Alzheimer's disease related cognitive functioning

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Aging 2015-12-01

There is an urgent need to develop molecular biomarkers of brain age in order to advance our understanding of age related neurodegeneration. 3 key findings →

Participants: 700 Evidence: low

Full summary, score breakdown and related studies → Original source

Identification of the Aβ37/42 peptide ratio in CSF as an improved Aβ biomarker for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2022-03-12

We conclude that the Aβ 37/42 ratio sensitively detects presenilin/γ-secretase dysfunction and better distinguishes CN from AD than Aβ42/40 in CSF. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Loss of nucleus basalis neurons containing trkA immunoreactivity in individuals with mild cognitive impairment and early Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of comparative neurology 2000-11-01

Recent studies indicate that there is a marked reduction in trkA-containing nucleus basalis neurons in end-stage Alzheimer's disease (AD). 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Apolipoprotein E epsilon4 allele, AD pathology, and the clinical expression of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neurology 2003-01-01

The APOE epsilon4 allele appears to be associated with the clinical manifestations of AD through an association with the pathologic hallmarks of AD rather than another mechanism. 5 key findings →

Participants: 77 Evidence: low

Full summary, score breakdown and related studies → Original source

Mixed Pathologies and Cognitive Outcomes in Persons Considered for Anti-Amyloid Treatment Eligibility Assessment: A Community-Based Study

✓ Peer-reviewed alzhub usefulness score 46 out of 100. Neurology 2025-08-18

Among 428 older autopsied persons (mean age at death = 91 years, 70% women) considered for anti-amyloid treatment eligibility assessment, 58% had MCI and 42% had mild-stage Alzheimer dementia. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Aβ mediates F-actin disassembly in dendritic spines leading to cognitive deficits in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-12-15

Dendritic spine structure is defined by filamentous actin (F-actin) and we observed depolymerization of synaptosomal F-actin accompanied by increased globular-actin (G-actin) at as early as 1 month of age in a mouse model of AD (APPswe/PS1ΔE9, male mice). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Glial heme oxygenase-1 expression in Alzheimer disease and mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 44 out of 100. Neurobiology of aging 2005-04-15

We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

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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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →

Newest studies, as a dated timeline →    Atom feed    Where this research is being discussed: events