Cerebral metabolism as measured with positron emission tomography (PET) and [18F] 2-deoxy-d-glucose: Healthy aging Alzheimer's disease and down syndrome

Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease

“…Meanwhile, compromised PDH function in 3xTg-AD neurons leads to a deficit in acetyl-CoA and consequently decreased OXPHOS activity as indicated by the decrease in OCR in 3xTg-AD neurons. These findings suggest a potential antecedent role of mitochondrial bioenergetic deficits in AD pathogenesis and are consistent with previous positron emission tomography (PET) metabolic analyses in persons with increased risk of AD, mild cognitive impairment (MCI), or incipient to late AD, in which decreased glucose uptake and utilization was demonstrated as among the earliest symptoms of AD occurring far before the onset of AD (24)(25)(26)(27). These findings are also consistent with microarray analyses of aging, incipient AD, and AD human samples and rodent models demonstrating that genes involved in mitochondrial bioenergetics are among those altered early in AD or MCI patients (22,28).…”

Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease

“…Meanwhile, compromised PDH function in 3xTg-AD neurons leads to a deficit in acetyl-CoA and consequently decreased OXPHOS activity as indicated by the decrease in OCR in 3xTg-AD neurons. These findings suggest a potential antecedent role of mitochondrial bioenergetic deficits in AD pathogenesis and are consistent with previous positron emission tomography (PET) metabolic analyses in persons with increased risk of AD, mild cognitive impairment (MCI), or incipient to late AD, in which decreased glucose uptake and utilization was demonstrated as among the earliest symptoms of AD occurring far before the onset of AD (24)(25)(26)(27). These findings are also consistent with microarray analyses of aging, incipient AD, and AD human samples and rodent models demonstrating that genes involved in mitochondrial bioenergetics are among those altered early in AD or MCI patients (22,28).…”

Possible Compensatory Events in Adult Down Syndrome Brain Prior to the Development of Alzheimer Disease Neuropathology: Targets for Nonpharmacological Intervention

“…These are characterized by small samples and a variety of scanning conditions so the results are sometimes inconsistent. For example, early reports on a small number of people with DS studied with PET and FDG showed higher cerebral glucose metabolic rate (GMR) than in non-trisomic individuals [33,163]. This was consistent with reports of cases of DS where higher than normal rates of synaptic density (and therefore more presumed neuronal activity) were found at autopsy [31,84].…”

The human genome is composed of viral DNA: Viral homologues of the protein products cause Alzheimer's disease and others via autoimmune mechanisms.

“…and PICALM, APOE4 and APOE among the top 70. Mitochondrial energy related proteins figured prominently among the top scorers likely explaining the reduction in cerebral glucose consumption prior to symtomatology in late-onset Alzheimer's disease 19 . Conversely, C.Neoformans was the pathogen scoring the greatest number of hits in relation to Alzheimer's disease proteins, by an order of magnitude.…”

Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease

“…Meanwhile, compromised PDH function in 3xTg-AD neurons leads to a deficit in acetyl-CoA and consequently decreased OXPHOS activity as indicated by the decrease in OCR in 3xTg-AD neurons. These findings suggest a potential antecedent role of mitochondrial bioenergetic deficits in AD pathogenesis and are consistent with previous positron emission tomography (PET) metabolic analyses in persons with increased risk of AD, mild cognitive impairment (MCI), or incipient to late AD, in which decreased glucose uptake and utilization was demonstrated as among the earliest symptoms of AD occurring far before the onset of AD (24)(25)(26)(27). These findings are also consistent with microarray analyses of aging, incipient AD, and AD human samples and rodent models demonstrating that genes involved in mitochondrial bioenergetics are among those altered early in AD or MCI patients (22,28).…”

Possible Compensatory Events in Adult Down Syndrome Brain Prior to the Development of Alzheimer Disease Neuropathology: Targets for Nonpharmacological Intervention

“…These are characterized by small samples and a variety of scanning conditions so the results are sometimes inconsistent. For example, early reports on a small number of people with DS studied with PET and FDG showed higher cerebral glucose metabolic rate (GMR) than in non-trisomic individuals [33,163]. This was consistent with reports of cases of DS where higher than normal rates of synaptic density (and therefore more presumed neuronal activity) were found at autopsy [31,84].…”

The human genome is composed of viral DNA: Viral homologues of the protein products cause Alzheimer's disease and others via autoimmune mechanisms.

“…and PICALM, APOE4 and APOE among the top 70. Mitochondrial energy related proteins figured prominently among the top scorers likely explaining the reduction in cerebral glucose consumption prior to symtomatology in late-onset Alzheimer's disease 19 . Conversely, C.Neoformans was the pathogen scoring the greatest number of hits in relation to Alzheimer's disease proteins, by an order of magnitude.…”

Mitochondrial bioenergetic deficit precedes Alzheimer's pathology in female mouse model of Alzheimer's disease

“…Meanwhile, compromised PDH function in 3xTg-AD neurons leads to a deficit in acetyl-CoA and consequently decreased OXPHOS activity as indicated by the decrease in OCR in 3xTg-AD neurons. These findings suggest a potential antecedent role of mitochondrial bioenergetic deficits in AD pathogenesis and are consistent with previous positron emission tomography (PET) metabolic analyses in persons with increased risk of AD, mild cognitive impairment (MCI), or incipient to late AD, in which decreased glucose uptake and utilization was demonstrated as among the earliest symptoms of AD occurring far before the onset of AD (24)(25)(26)(27). These findings are also consistent with microarray analyses of aging, incipient AD, and AD human samples and rodent models demonstrating that genes involved in mitochondrial bioenergetics are among those altered early in AD or MCI patients (22,28).…”

Possible Compensatory Events in Adult Down Syndrome Brain Prior to the Development of Alzheimer Disease Neuropathology: Targets for Nonpharmacological Intervention

“…These are characterized by small samples and a variety of scanning conditions so the results are sometimes inconsistent. For example, early reports on a small number of people with DS studied with PET and FDG showed higher cerebral glucose metabolic rate (GMR) than in non-trisomic individuals [33,163]. This was consistent with reports of cases of DS where higher than normal rates of synaptic density (and therefore more presumed neuronal activity) were found at autopsy [31,84].…”

The human genome is composed of viral DNA: Viral homologues of the protein products cause Alzheimer's disease and others via autoimmune mechanisms.

“…and PICALM, APOE4 and APOE among the top 70. Mitochondrial energy related proteins figured prominently among the top scorers likely explaining the reduction in cerebral glucose consumption prior to symtomatology in late-onset Alzheimer's disease 19 . Conversely, C.Neoformans was the pathogen scoring the greatest number of hits in relation to Alzheimer's disease proteins, by an order of magnitude.…”