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1 aptic breakdown, cell death, and devastating memory loss.
2 cation, often before the appearance of overt memory loss.
3 FMS and 43 control subjects) presenting with memory loss.
4 is recurrent, transient episodes of isolated memory loss.
5 elated the levels of these tau proteins with memory loss.
6 ue in diseases and conditions that result in memory loss.
7 at might point to the mechanisms behind such memory loss.
8 fluence its ability to reduce age-associated memory loss.
9 (AD) characteristically presents with early memory loss.
10 lderly patients who present with symptoms of memory loss.
11 ng apart neural mechanisms underlying remote memory loss.
12 sease; the initial phase is characterized by memory loss.
13 olimus had no effect on seizure frequency or memory loss.
14 dementia characterized by mental slowing and memory loss.
15 pathway is defective in age-related spatial memory loss.
16 its will allow future targeted treatment for memory loss.
17 d psychological effects in humans, including memory loss.
18 ession to dementia in patients with isolated memory loss.
19 s provided clearcut evidence of time-related memory loss.
20 sequilibrium, neck stiffness, dysphagia, and memory loss.
21 release, failure of synaptic plasticity, and memory loss.
22 can be further explored in a mouse model of memory loss.
23 l conditions such as depression, anxiety and memory loss.
24 oid production, tau hyperphosphorylation and memory loss.
25 pression in either MBn or DAn impairs normal memory loss.
26 er's disease (AD) and related tauopathies is memory loss.
27 the brain leads to differential patterns of memory loss.
28 ndependently of Abeta, eventually leading to memory loss.
29 where olfactory deficits precede detectable memory loss.
30 C, was sufficient to produce METH-associated memory loss.
31 , and LTP dysfunction is thought to underlie memory loss.
32 polymerization contributes to age-associated memory loss.
33 ign of preclinical AD and may predict future memory loss.
34 astrocytic A2A receptor levels contribute to memory loss.
35 but this dysfunction was not associated with memory loss.
36 in aged flies protected against APP-induced memory loss.
37 s of Alzheimer's disease (AD) and consequent memory loss.
38 de as senile plaques, neurodegeneration, and memory loss.
39 ressive neurodegenerative disease leading to memory loss.
40 nsulin signaling, synapse deterioration, and memory loss.
41 rtex, as a substrate of age-related episodic-memory loss.
42 luded depression, explosivity and short-term memory loss.
43 plaques, progressive neurodegeneration, and memory loss.
44 which is potentially linked to age-dependent memory loss.
45 ermines the pattern and extent of retrograde memory loss?
46 ities (1.6 [1.5-1.8]), pain (1.6 [1.5-1.7]), memory loss (1.8 [1.6-2.0]), dizziness (1.7 [1.6-1.8]),
48 se sensitivity (12.0 vs 3.0 days, P = .004), memory loss (9.0 vs 4.0 days, P = .04), nausea (9.0 vs 3
49 ys or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally
50 cally solvable quantum model describing this memory loss across an integrability-chaos transition und
52 se series of patients with acute psychogenic memory loss (also known as dissociative/functional amnes
53 amates using a model of amyloid beta induced memory loss and a transgenic mouse model of Alzheimer's
54 interpretation of these results, namely that memory loss and Abeta(insol) were closely connected, was
56 tion or short durations of INO prevents this memory loss and also attenuates the inflammatory respons
58 , which were correlated with the reversal of memory loss and anxiety-like behavior observed in APP/PS
61 n cause of dementia, and is characterized by memory loss and cognitive decline, as well as amyloid be
64 ission in this pathway may be related to the memory loss and dementia that accompanies normal aging a
66 81 on tau, identified in AD brains, promotes memory loss and disrupts synaptic plasticity by reducing
67 gnaling pathways but accelerates the rate of memory loss and exacerbates mitochondrial dysfunction in
68 0.78, 2.2], and a symptom cluster including memory loss and finger tremor (OR 14, 95% CI: 3.5, 57).
73 the activation of Wnt signaling also rescues memory loss and improves synaptic dysfunction in APP/PS1
75 in the adult mouse brain causes progressive memory loss and neurodegeneration resembling AD, whereas
78 tellectual dysfunction began with subjective memory loss and objective visuospatial dysfunction and w
81 rinic signaling using M1 mAChR PAMs restored memory loss and slowed the progression of mouse prion di
83 , 10 subjects developed symptoms of episodic memory loss and subsequently progressed to fulfil criter
84 gests that ginkgo is of questionable use for memory loss and tinnitus but has some effect on dementia
85 pocampal dysfunction (i.e. severe short-term memory loss) and three with extensive limbic dysfunction
87 ss is known to induce cognitive impairments, memory loss, and neurodegeneration owing to its potent D
96 e tau multimers correlated consistently with memory loss at various ages in the rTg4510 mouse model.
97 The natural history of patients with severe memory loss but no other type of cognitive impairment is
98 rong relationship between greater stress and memory loss, but few studies have examined this relation
99 our inquiry into the molecular basis of this memory loss by studying Abeta42-induced enhancement of l
101 following demonstration that Abeta42-induced memory loss can be rescued through genetic silencing or
103 ent reports provided substantial evidence of memory loss, cognitive decline, and dementia related to
104 Alzheimer's disease (AD) is characterized by memory loss, cognitive decline, and devastating neurodeg
105 subsequent development of disorders such as memory loss, cognitive decline, seizures, and epilepsy.
106 severity and 2) controls with no subjective memory loss complaints and a score >30 in the Phototest
109 cade in both AD- and Down's syndrome-related memory loss could be triggered by alterations in APP pro
110 disciplinary article compares the pattern of memory loss described in Gabriel Garcia Marquez's One Hu
111 w-up, 48% (n = 10) of patients with isolated memory loss-developed dementia compared with 18% (n = 36
113 en vestibular vertigo, cognitive impairment (memory loss, difficulty concentrating, confusion) and ps
114 ataxia of gait, in the hemizygote group; and memory loss, dizziness, ataxia, hemiparesis, loss of con
115 umbers of BIS-depressed readings and percent memory loss during sedation, while reducing total diazep
116 results provide a candidate explanation for memory losses during normal aging and indicate that, wit
118 Other documented symptoms were short-term memory loss, executive function deficits, cognitive decl
119 ional documented symptoms include short-term memory loss, executive functional deficits, cognitive de
120 We found that our patients with psychogenic memory loss fell into four distinct groups, which we cat
122 age, sex, education level, and self reported memory loss, for the development of depression were 6.5
124 ich often entails cognitive disturbances and memory loss, has become a major complication for lupus p
126 0-101 years]; P = .29), presenting symptoms (memory loss in 7 of 7 mutation carriers [100%] vs 958 of
127 mory retention in normal animals and reduced memory loss in a murine model of Alzheimer's disease.
128 for transcriptional changes underlying early memory loss in AD by examining pathological, behavioral,
129 Abeta assemblies contribute significantly to memory loss in AD, then successfully targeting them migh
137 Consequently, research into the causes of memory loss in Alzheimer's disease continues to centre o
140 beta42 stimulates PI3K, which in turn causes memory loss in association with an increase in accumulat
143 lication of this paradigm of Abeta42-induced memory loss in Drosophila to investigate the protective
144 upregulation may contribute to age-dependent memory loss in DS and AD and points to correcting calcin
145 Synapse deterioration underlying severe memory loss in early Alzheimer's disease (AD) is thought
148 ed with estrogen depletion, including verbal memory loss in humans, may therefore stem from compromis
149 een established in deterministic models, and memory loss in learning has been seen to act similarly t
150 ignificant correlate of clinical severity of memory loss in mild cognitive impairment (P < .001).
151 potential mechanisms for therapies to combat memory loss in normal cognitive aging and dementia.
156 ignificant, gradually progressive short-term memory loss in the absence of any history of strokes or
160 nd novel object recognition tests, and their memory loss in the novel object recognition test is asso
162 endent deficits were eliminated, we detected memory loss in transgenic mice expressing mutant APP (Tg
164 Thus, the clinical defects of learning and memory loss in vivo in GPI(-/-) PrP tg mice infected wit
165 are thought to instigate synapse damage and memory loss, induce depressive-like behavior in mice.
166 health complications include neurotoxicity, memory loss, infertility in males, and development of a
167 decline was similar in both families: early memory loss (initially selective for verbal memory in so
168 ography (FDG-PET) associated with short-term memory loss, insomnia, and temporal lobe electrographic
171 nt attempts to describe those people in whom memory loss is not of such severity to merit a diagnosis
175 sruption of neural activity can also lead to memory loss, it may be that memory permanence is mediate
176 ghts into the molecular basis of age-related memory loss may hold promise for new treatments for cogn
178 observed associations of TDP-43 with greater memory loss, naming and functional decline, and smaller
180 mory deficits similar to FDD(KI/+) mice, and memory loss of FDD(KI/+) mice is prevented by expression
182 ovelty exposure prevented the stress-induced memory loss of the spatial task and increased BDNF and A
183 complaints, 21 patients with severe isolated memory loss of unknown cause were identified and followe
184 ovel view of the effects of tau and Abeta on memory loss, offering new therapeutic opportunities in t
186 CI 1.2-3.6; p=0.008) and limitations due to memory loss or confusion (PR 5.8, 1.5-22.4; p=0.010) wer
187 omen, 14 men) with difficult-to-characterize memory loss or dementia (using standard clinical criteri
188 teristic features of Alzheimer's disease are memory loss, plaques resulting from abnormal processing
191 erative disorder associated with progressive memory loss, severe dementia, and hallmark neuropatholog
193 e neurodegenerative disorder with associated memory loss, spatial disorientation, and other psychiatr
198 eimer's disease While the findings show that memory loss usually exceeds executive dysfunction in pat
199 By preventing measles-associated immune memory loss, vaccination protects polymicrobial herd imm
201 sexecutive symptoms; and for three patients, memory loss was accompanied by apathy but no other behav
202 oss was the only complaint; for one patient, memory loss was accompanied by personality change; for t
203 ied by personality change; for two patients, memory loss was accompanied by prominent dysexecutive sy
205 ical and molecular mechanisms of age-related memory loss, we assessed spatial memory in C57BL/B6 mice
206 a colloid cyst, a condition associated with memory loss when accompanied by fornix and/or mammillary
207 eneralization to a novel environment show no memory loss when the hippocampus is subsequently inactiv
208 tion, accumulation of lipofuscin bodies, and memory loss, whereas their cortical and hippocampal neur
209 y many PD patients, including depression and memory loss, which do not respond well to currently avai
211 ports from an informant that the patient has memory loss yields an LR of 6.5 (95% CI, 4.4-9.6) for de
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