"SPECT and PET are able to detect regional hypoperfusion/hypometabolism in a biparietal and bitemporal distribution, while amyloid and tau agents accumulate in the grey matter and medial temporal lobes, respectively19."
"apolipoprotein E (ApoE) ε4 (epsilon 4) allele carrier status 21"
"A clinical diagnosis can be made by identifying a progressive decline in memory both with clinical examinations and neuropsychologic tests and has been historically based on the NINCDS-ADRDA criteria, which divides patients according to the certainty of the diagnosis into 5:"
"Importantly, the NINCDS-ADRDA criteria include imaging and laboratory examination, or blood and CSF, to exclude other causes."
"These measures have been combined in the medial temporal atrophy score, which has been shown to be predictive of progression from mild cognitive impairment (MCI) to dementia 5,6. Another described alternative is the entorhinal cortical atrophy score (ERICA score)."
"partial NMDA receptor antagonists, e.g., memantine"
"aducanumab (discontinued in 2024 after initial FDA approval)"
"amyloid-lowering monoclonal antibodies were FDA-approved using criteria based on T2* sequences, and not SWI sequences 29"
"Amyloid-lowering monoclonal antibodies may result in the complication of amyloid-related imaging abnormalities (ARIA), which can result in haemorrhage (ARIA-H) or oedema (ARIA-E), the latter is closely related to cerebral amyloid angiopathy related inflammation 20."
"Amyloid-lowering monoclonal antibodies may result in the complication of amyloid-related imaging abnormalities (ARIA), which can result in haemorrhage (ARIA-H) or oedema (ARIA-E), the latter is closely related to cerebral amyloid angiopathy related inflammation 20."
"In cases where bilateral mesial temporal lobe volume loss is present on imaging in an elderly amnestic patient, the main differential is limbic-predominant age-related TDP-43 encephalopathy (LATE) 11,25. Not only is this entity increasingly recognised as a significant cause of dementia of Alzheimer type despite being pathologically distinct, but it can also co-exist with Alzheimer disease 11. There is no definitive way of establishing the diagnosis other than retrospectively at autopsy; however, a number of features may suggest the diagnosis 11:"
"Classical/typical Alzheimer disease"
"Early-onset Alzheimer disease"
"Atypical/variant Alzheimer disease"
"PET agents that bind tau proteins in neurofibrillary tangles are being investigated (e.g. F-18 flortaucipir, trade name Tauvid), which result in increased activity in the expected locations of deposition in Alzheimer disease (hippocampus, entorhinal cortex and temporal and parietal cortex) 7,10. They correlate with the severity of dementia/cognitive impairment but are, however, not specific to Alzheimer disease and will also deposit in other tauopathies (e.g., chronic traumatic encephalopathy and progressive supranuclear palsy) 10,19."
"cholinesterase inhibitors, e.g. donepezil, rivastigmine, and galantamine"
Expected headings
"Biomarker diagnosis"
"Clinical diagnosis"
"Classical/typical Alzheimer disease"
"Early-onset Alzheimer disease"
"Atypical/variant Alzheimer disease"
"FDG-PET"
"Amyloid PET"
"Tau PET"
"Complications"
"The underlying reason for the accumulation of senile (neuritic) plaques and neurofibrillary tangles remains poorly understood, as does the reason for non-uniform distribution in the cortex. There is, however, increasing evidence to suggest that chronic inflammation is at least partially responsible. Such inflammation can lead to prolonged parenchymal activation of microglial cells, which in turn results in the release of inflammatory mediators with subsequent neuronal damage and amyloid-induced neurodegeneration 12."
"There is no cure for this disease; some drugs have been developed trying to improve symptoms or, at least, temporarily slow down their progression."
"In cases where bilateral mesial temporal lobe volume loss is present on imaging in an elderly amnestic patient, the main differential is limbic-predominant age-related TDP-43 encephalopathy (LATE) 11,25. Not only is this entity increasingly recognised as a significant cause of dementia of Alzheimer type despite being pathologically distinct, but it can also co-exist with Alzheimer disease 11. There is no definitive way of establishing the diagnosis other than retrospectively at autopsy; however, a number of features may suggest the diagnosis 11:"
"C-11 Pittsburgh compound B (half-life 20 minutes), as well as newer longer half-life compounds such as F-18 florbetapir (trade name Amyvid), F-18 flutemetamol (trade name Vizamyl), and F-18 florbetaben (trade name NeuraCeq), are PET tracers that bind preferentially to beta-amyloid fibrils and thus may be able to improve the specificity of antemortem diagnosis 8,9, although there is considerable overlap with normal controls 2,7. Additionally, it should be noted that the degree of amyloid deposition does not correlate with the degree of cognitive impairment 19."
"C-11 Pittsburgh compound B (half-life 20 minutes), as well as newer longer half-life compounds such as F-18 florbetapir (trade name Amyvid), F-18 flutemetamol (trade name Vizamyl), and F-18 florbetaben (trade name NeuraCeq), are PET tracers that bind preferentially to beta-amyloid fibrils and thus may be able to improve the specificity of antemortem diagnosis 8,9, although there is considerable overlap with normal controls 2,7. Additionally, it should be noted that the degree of amyloid deposition does not correlate with the degree of cognitive impairment 19."
"There is no cure for this disease; some drugs have been developed trying to improve symptoms or, at least, temporarily slow down their progression."
"In cases where bilateral mesial temporal lobe volume loss is present on imaging in an elderly amnestic patient, the main differential is limbic-predominant age-related TDP-43 encephalopathy (LATE) 11,25. Not only is this entity increasingly recognised as a significant cause of dementia of Alzheimer type despite being pathologically distinct, but it can also co-exist with Alzheimer disease 11. There is no definitive way of establishing the diagnosis other than retrospectively at autopsy; however, a number of features may suggest the diagnosis 11:"
"History and etymology"