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Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Highest usefulness score first. Studies without a score come last.

  1. Quantifying mRNA in postmortem human brain: influence of gender, age at death, postmortem interval, brain pH, agonal state and inter-lobe mRNA variance

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 2003-10-01 Biomarkers

    The quantification of mRNA in postmortem human brain is often made complicated by confounding factors.

  2. Proteomic studies of potential cerebrospinal fluid protein markers for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 2003-10-01 Genetics

    By comparing the cerebrospinal fluid (CSF) proteome between Alzheimer's disease (AD) patients and controls, it may be possible to identify proteins that play a role in the disease process and thus to study the pathogenesis of AD.

  3. Biochemical markers related to Alzheimer's dementia in serum and cerebrospinal fluid

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 2002-07-01 Biomarkers

    The diagnosis of Alzheimer's disease (AD) is currently based on clinical and neuropsychological examination.

  4. Increase of brain oxidative stress in mild cognitive impairment: a possible predictor of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Archives of neurology 2002-06-01 Tau biomarkers

    These results imply that individuals with MCI have increased brain oxidative damage before the onset of symptomatic dementia.

  5. Neurofilament protein in cerebrospinal fluid: a marker of white matter changes

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuroscience research 2001-11-01 Biomarkers

    The objective of this study was to compare cerebrospinal fluid (CSF) levels of the light subtype of the neurofilament proteins (NFL), tau, and beta-amyloid42 (Abeta42) in individuals with moderate or severe white matter changes (WMC) and in those with mild or no WMC.

  6. Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of clinical investigation 2000-12-01 Genetics

    Elimination of amyloid-ss peptide (Ass) from the brain is poorly understood.

  7. X-34, a fluorescent derivative of Congo red: a novel histochemical stain for Alzheimer's disease pathology

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society 2000-09-01 Drug development

    X-34, a lipophilic, highly fluorescent derivative of Congo red, was examined as a histochemical stain for pathological changes in Alzheimer's disease (AD).

  8. Early amyloid deposition in the medial temporal lobe of young Down syndrome patients: a regional quantitative analysis

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Experimental neurology 1998-04-01 Down syndrome and Alzheimer's

    The presence of the neuropathological alterations of Alzheimer's disease (AD) in essentially all older Down syndrome (DS) patients suggests that the examination of younger DS patients may clarify the early pathological progression of AD.

  9. Serum interleukin-6 levels correlate with the severity of dementia in Down syndrome and in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Acta neurologica Scandinavica 1997-10-01 Down syndrome and Alzheimer's

    These findings suggest a disease stage dependent general activation of the immune system both in sporadic AD and in DS with AD.

  10. Diagnostic criteria for neuropathologic assessment of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 1997-07-01 Getting a diagnosis

    Prior to any evaluation of morphologic brain changes, a decision must be made whether a given alteration is associated with aging or with disease.

  11. Analysis of heterogeneous A4 peptides in human cerebrospinal fluid and blood by a newly developed sensitive Western blot assay

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1996-09-01 Tau biomarkers

    The betaA4 peptide, a major component of senile plaques in Alzheimer's disease (AD) brain, has been found in cerebrospinal fluid (CSF) and blood of both AD patients and normal subjects.

  12. Retinal pathology in Alzheimer's disease. I. Ganglion cell loss in foveal/parafoveal retina

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 1996-05-01 Brain scans and imaging

    Morphometric analysis of the numbers of neurons in the ganglion cell layer (GCL) of the central retina (fovea/foveola/parafoveal retina) in eyes from 9 Alzheimer's disease (AD) and 11 age-matched control cases revealed an overall decrease of 25% in total numbers of neurons in AD as compared with control eyes.

  13. Amyloid beta protein (A beta) in Alzheimer's disease brain. Biochemical and immunocytochemical analysis with antibodies specific for forms ending at A beta 40 or A beta 42(43)

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1995-03-01 Tau biomarkers

    Biochemical and immunocytochemical analyses were performed to evaluate the composition of the amyloid beta protein (A beta) deposited in the brains of patients with Alzheimer's disease (AD).

  14. beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1993-11-01 Vascular contributions

    Reinvestigation of the chemical structure of beta-amyloid peptide (A beta) deposits in the vascular tissue of Alzheimer disease brains revealed that the 42-residue form A beta-(1-42), rather than the more soluble A beta-(1-40) form, is the predominant peptide.

  15. The lack of accumulation of senile plaques or amyloid burden in Alzheimer's disease suggests a dynamic balance between amyloid deposition and resolution

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 1993-11-01 Down syndrome and Alzheimer's

    A beta, a nearly insoluble peptide, is generally assumed to irreversibly deposit and accumulate as senile plaques (SP) during the course of Alzheimer's disease (AD).

  16. Hydrated autoclave pretreatment enhances tau immunoreactivity in formalin-fixed normal and Alzheimer's disease brain tissues

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Laboratory investigation; a journal of technical methods and pathology 1991-05-01 Drug development

    We developed a new immunohistochemical method by which normal tau antigenicity can be visualized in paraffin sections of formalin-fixed brain tissue.

  17. Constant neurofibrillary changes in the neocortex in progressive supranuclear palsy. Basic differences with Alzheimer's disease and aging

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience letters 1990-11-01 Drug development

    Neocortical neurofibrillary tangles (NFT) revealed by Bodian technique and anti-tau immunolabelling were seen in 5/5 cases of progressive supranuclear palsy (PSP) aged 58-76 years.

  18. Optic nerve damage in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Ophthalmology 1990-01-01 Brain scans and imaging

    Optic nerves from ten patients with Alzheimer's disease were histologically examined and compared with those from age-matched controls.

  19. Retinal ganglion cell degeneration in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research 1989-11-01 Brain scans and imaging

    This study documents the light-microscopic and ultrastructural characteristics of ganglion cell degeneration in the retinas of patients with Alzheimer's disease (AD).

  20. Patterns of gliosis in Alzheimer's disease and aging cerebrum

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Glia 1989-01-01 Biomarkers

    The distribution of astrocytic gliosis in Alzheimer's disease (AD) and aging cerebrum, as marked by immunoperoxidase staining for glial fibrillary acidic protein (GFAP), was examined in whole-hemisphere coronal sections.

  21. Tumor diagnosis by intermediate filament typing: a novel tool for surgical pathology

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Laboratory investigation; a journal of technical methods and pathology 1983-04-01 Biomarkers

    In most cell types intermediate or 10-mm filaments (IF) are a major cytoskeletal organization and, thus, directly or indirectly influence the structural appearance of the cytoplasm.

  22. Biochemical Assessment of Serotonergic and Cholinergic Dysfunction and Cerebral Atrophy in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of Neurochemistry 1983-01-01 Disease mechanisms

    Markers of serotonin synapses in entire temporal lobe and frontal and temporal neocortex were examined for changes in Alzheimer's disease by use of both neurosurgical and autopsy samples.

  23. Delayed radiation necrosis of the brain

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurosurgery 1977-09-01 Risk factors

    The cases of six patients are presented to delineate the clinical profile of delayed radiation necrosis of the brain.

  24. Colloid cysts of the third ventricle

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurosurgery 1974-02-01 Digital health tools

    ✓ Thirty-eight cases of colloid cyst of the third ventricle are reviewed.

  25. Longitudinal plasma biomarkers and multimodal PET across APOE ε4 genotypes: a prospective cohort study

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-11-01 Biomarkers

    These findings support a model in which p-tau217 specifically tracks amyloid-driven pathological progression, while markers of neurodegeneration reflect broader age-related processes that are not associated with APOE genotype.

From across this topic

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