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Cognitive decline

About: Cognitive decline is a research topic. Over the lifetime, 29308 publications have been published within this topic receiving 1174689 citations.


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Journal ArticleDOI
TL;DR: Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.
Abstract: Summary Epileptic activity is frequently associated with Alzheimer's disease; this association has therapeutic implications, because epileptic activity can occur at early disease stages and might contribute to pathogenesis. In clinical practice, seizures in patients with Alzheimer's disease can easily go unrecognised because they usually present as non-motor seizures, and can overlap with other symptoms of the disease. In patients with Alzheimer's disease, seizures can hasten cognitive decline, highlighting the clinical relevance of early recognition and treatment. Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disease, detected by extended neurophysiological monitoring, can also lead to accelerated cognitive decline. Treatment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AEDs), in low doses, is usually well tolerated and efficacious. Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties. These AEDs target mechanisms of epileptogenesis involving amyloid β and tau. Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.

346 citations

Journal ArticleDOI
01 Nov 2004-Stroke
TL;DR: The vascular factors that might be responsible to cognitive decline in Alzheimer disease and vascular cognitive impairment are reviewed and the corresponding intervenvations that might prevent cognitive impairment as the authors age are reviewed.
Abstract: Alzheimer disease and vascular cognitive impairment are important causes of cognitive decline in the elderly. It has now been shown that vascular risk factors have measurable negative effects on the brain and are associated with cognitive impairment. We review vascular factors that might be responsible to cognitive decline in Alzheimer disease and vascular cognitive impairment and the corresponding intervenvations that might prevent cognitive impairment as we age.

345 citations

Journal ArticleDOI
TL;DR: Evidence is added that inflammation against Aβ can cause vascular dysfunction, a potential mechanism for the toxic response recently observed in clinical trials of Aβ immunization.
Abstract: To explore the clinical effects of inflammation associated with vascular deposits of the amyloid beta peptide (A beta), we analyzed 42 consecutive patients with pathologically diagnosed cerebral amyloid angiopathy (CAA) for evidence of an inflammatory response. Inflammation with giant-cell reaction surrounding amyloid-laden vessels was identified in 7 of the 42 cases. The clinical symptoms in each of the seven were subacute cognitive decline or seizure rather than hemorrhagic stroke, the primary clinical presentation in 33 of 35 patients with noninflammatory CAA (p < 0.001). Inflammatory CAA also was associated with radiographic white matter abnormalities, significantly younger age at presentation, and a marked overrepresentation of the apolipoprotein E epsilon 4/epsilon 4 genotype (71% vs 4%, p < 0.001). Of the six inflammatory CAA patients with available follow-up information, five demonstrated clinical and radiographic improvement after immunosuppressive treatment. The syndrome of CAA-related perivascular inflammation appears to represent a subset of CAA with clinically distinct symptoms that may respond to immunosuppressive treatment. These data add to evidence that inflammation against A beta can cause vascular dysfunction, a potential mechanism for the toxic response recently observed in clinical trials of A beta immunization.

345 citations

Journal ArticleDOI
TL;DR: To determine survival, functional independence, and cognitive performance of older patients 2 years after an episode of delirium, a large number of patients are referred to a single hospital for evaluation of their mental and physical health.
Abstract: Objective To determine survival, functional independence, and cognitive performance of older patients 2 years after an episode of delirium. Design Descriptive cohort study. Setting General medical wards of a teaching hospital. Patients Two hundred twenty-nine consecutive patients aged 70 years or older who had been community-dwelling prior to admission. Fifty patients met criteria for delirium (cases); these were compared to patients without delirium (controls). Two-hundred twenty-three patients survived hospitalization (46 cases, 177 controls) Of these, 92% were followed greater than or equal to 2 years. Main outcome measures Vital status, place of residence, activities of daily living (ADL), and cognitive performance were determined by telephone interview of patients or care-givers 2 years after discharge. Independent community living was defined as survivorship outside of an institution and without dependence in any of four basic ADL (bathing, dressing, transfers, eating). Results Two-year mortality in the entire population was 39% for cases and 23% for controls (relative risk 1.82, 95% confidence interval 1.04-3.19). Delirium identified those patients at risk for loss of independent community living, even after adjustment for potential confounding variables (adjusted odds ratio 2.56, 95% confidence interval 1.10-5.91). Follow-up cognitive testing in a subset of patients with high baseline performance revealed a greater decline in performance among cases of delirium than controls (P = 0.023). Conclusions Delirium identifies older patients at risk for mortality or loss of independence. Delirium may also identify patients at risk for future cognitive decline.

345 citations

Journal ArticleDOI
TL;DR: A central role for mitochondria in neurodegeneration is suggested and evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative stress and metabolic failure, namely AD is provided.
Abstract: Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the progression of Alzheimer's disease (AD). We examined the ability of the novel mitochondria-targeted antioxidant MitoQ (mitoquinone mesylate: [10-(4,5-dimethoxy-2-methyl-3,6-dioxo-1,4-cycloheexadienl-yl) decyl triphenylphosphonium methanesulfonate]) to prevent AD-like pathology in mouse cortical neurons in cell culture and in a triple transgenic mouse model of AD (3xTg-AD). MitoQ attenuated β-amyloid (Aβ)-induced neurotoxicity in cortical neurons and also prevented increased production of reactive species and loss of mitochondrial membrane potential (Δψ(m)) in them. To determine whether the mitochondrial protection conferred by MitoQ was sufficient to prevent the emergence of AD-like neuropathology in vivo, we treated young female 3xTg-AD mice with MitoQ for 5 months and analyzed the effect on the progression of AD-like pathologies. Our results show that MitoQ prevented cognitive decline in these mice as well as oxidative stress, Aβ accumulation, astrogliosis, synaptic loss, and caspase activation in their brains. The work presented herein suggests a central role for mitochondria in neurodegeneration and provides evidence supporting the use of mitochondria-targeted therapeutics in diseases involving oxidative stress and metabolic failure, namely AD.

344 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
2023914
20221,895
20213,389
20202,982
20192,551
20182,022