Frontotemporal dementia with parkinsonism, chromosome 17 type (FTDP-17), a recently defined disease entity, is clinically characterized by personality changes sometimes associated with psychosis, hyperorality, and diminished speech output, disturbed executive function and nonfluent aphasia, bradykinesia, and rigidity. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
Full text may need a subscription
Clinical data alone poorly predicted phenoconversion in RBD due to synucleinopathy patients. 3 key findings →
Participants: 173
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
The term frontotemporal dementia (FTD) encompasses a range of clinical syndromes that are believed not to map reliably onto the spectrum of recognized pathologies. 2 key findings →
Participants: 61
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Cerebral blood flow (CBF) velocity is decreased in patients with Alzheimer's disease. 4 key findings →
Participants: 1,716
Evidence: low
Full summary, score breakdown and related studies →
Original source
Full text may need a subscription
Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. 2 key findings →
Participants: 28
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Subtle memory impairment with a positive β-amyloid scan identifies healthy individuals at high risk for MCI or AD. 3 key findings →
Participants: 87
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
Our data suggest that [F-18]-AV-1451 holds promise as a surrogate marker for the detection of brain tau pathology in the form of tangles and paired helical filament-tau-containing neurites in Alzheimer brains but also point to its relatively lower affinity for lesions primarily made of straight tau filaments in non-Alzheimer tauopathy cases and to the existence of some [F-18]-AV-1451 off-target binding. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Although olfactory dysfunction is commonly associated with Parkinson's disease (PD), it is not known whether such dysfunction can predate the onset of clinical PD in a community-based population. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Full text may need a subscription
Niney-two PD patients developed dementia, and 48 remained cognitively normal. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
CBD was associated with 4 clinical syndromes: progressive nonfluent aphasia (n = 5), behavioral variant frontotemporal dementia (n = 5), executive-motor (n = 7), and posterior cortical atrophy (n = 1). 2 key findings →
Participants: 18
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
18 F-flortaucipir uptake was elevated in PSP versus controls and PD patients in a pattern consistent with the expected distribution of tau pathology. 3 key findings →
Participants: 33
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Parietal and occipital lobar CMBs counts were higher in PiB(+) ADCI with moderate WMH than PiB(+) ADCI with minimal WMH, whereas PiB(-) patients with SVCI (ie, "pure" SVCI) showed both lobar and deep CMBs. 3 key findings →
Participants: 226
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
These findings suggest that CSF VILIP-1 and VILIP-1/Aβ42 offer diagnostic utility for early AD, and can predict future cognitive impairment in cognitively normal individuals similarly to tau and tau/Aβ42, respectively. 3 key findings →
Participants: 211
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
Covert cerebrovascular disease and its consequences on cognitive and gait performance and brain atrophy are manifest in some clinically asymptomatic persons as early as the 5th decade of life. 3 key findings →
Participants: 803
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
LBD patients with AD copathology harbor greater neocortical SYN pathology. 1 key finding →
Participants: 36
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
Our PET study replicated postmortem spreading patterns of tau and amyloid-β pathologies. 1 key finding →
Participants: 195
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Triggering receptor expressed on myeloid cells-2 (TREM2) and progranulin (PGRN) are critical regulators of microglia activation and can be detected in cerebrospinal fluid (CSF). 4 key findings →
Design: longitudinal study
Participants: 65
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
Magnetic resonance (MR) imaging is used widely for assessment of patients with cognitive impairment, but the pathological correlates are unclear, especially when multiple pathologies are present. 4 key findings →
Participants: 93
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
Although previous research has shown that initiation of postmenopausal estrogen hormone therapy (HT) in late life increases risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial; however, this has not been rigorously investigated in large population-based studies. 4 key findings →
Participants: 1,524
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
Analyses revealed significant nonlinear interaction effects of ELS severity and age on NfL and GFAP serum concentrations, total and subcortical gray matter volume loss, increased third ventricular volume, and cognitive impairment. 3 key findings →
Participants: 179
Evidence: low
Full summary, score breakdown and related studies →
Original source
Free full text
In ARIC (n = 1,736, mean age 63, 58.8% female, 48.7% non-Hispanic White individuals, median follow-up 18.6 years), the dementia incidence rate was 10.4 (95% CI, 9.2-11.6) per 1,000 person-years. 5 key findings →
Design: cohort study
Participants: 1,736
Evidence: moderate
Full summary, score breakdown and related studies →
Original source
Free full text
The distribution and density of neurofibrillary tangles and amyloid plaques was studied in a unique series of cases whose premortem cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very mildly demented cases (CDR = 0.5), and 8 severely demented (CDR = 3) cases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies →
Original source
Full text may need a subscription
Compared with healthy controls, patients with ALS - particularly those with cognitive impairment (ALSci) or ALS-FTD - showed elevated AD-related biomarkers. 5 key findings →
Participants: 192
Evidence: low
Full summary, score breakdown and related studies →
Original source
We found strong evidence that plasma p-tau 181 is elevated in ALS and may be a novel marker specific to LMN dysfunction. 4 key findings →
Participants: 130
Evidence: low
Full summary, score breakdown and related studies →
Original source
This is the first report describing Aβ-PF species captured by lecanemab in human CSF and supporting that Lec-PF is correlated with neurodegeneration in AD and may explain the mechanism of the clinical effect of lecanemab. 3 key findings →
Participants: 163
Evidence: low
Full summary, score breakdown and related studies →
Original source
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 30,980 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.