ライフサイエンスコーパス: memory disorder

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1 vocabulary development were arrested by his memory disorder.

2 ble to probe the biological underpinnings of memory disorders.

3 , offering promise for targeted treatment of memory disorders.

4 t clinical implications for the treatment of memory disorders.

5 tion as treatment strategies for maladaptive memory disorders.

6 with those working primarily in the area of memory disorders.

7 it may be useful for treating patients with memory disorders.

8 s received little attention in patients with memory disorders.

9 uld contribute to FAS and ethanol-associated memory disorders.

10 tially relevant to synaptic malplasticity or memory disorders.

11 understanding of human cognition and related memory disorders.

12 s, a key region associated with epilepsy and memory disorders.

13 lities for degenerative and neuropsychiatric memory disorders.

14 H2A.Z as a potential therapeutic target for memory disorders.

15 diagnostic subtypes of MCI have an episodic memory disorder (amnestic MCI) occurring either alone [s

16 patients consulting their GP with suspected memory disorders and proportion of those referred to mem

17 hold the key to understanding the variety of memory disorders associated with aging and disease.

18 e inconsistent with Mendelian segregation of memory disorders both in families of affected probands w

19 We studied patients who attended the Duke Memory Disorders Clinic and were diagnosed as having pro

20 evidence that the pattern of transmission of memory disorders differs in nuclear families in which th

21 In humans, the most conspicuous memory disorder following vmPFC damage is confabulation;

22 ral lobe seizures in 16 patients (88.9%) and memory disorders in 17 patients (94.4%) from the cohort.

23 s in the hippocampus may conceivably lead to memory disorders in the mammalian brain.

24 P consultations with patients with suspected memory disorders increased in intervention versus contro

25 e huge motivation to treat age-related human memory disorders, interaction between human CA3 and dent

26 It thus appears that, if this selective memory disorder is a special syndrome related to the ear

27 ship of gene expression changes to memory or memory disorders is not well understood.

28 ble to probe the biological underpinnings of memory disorders marked by impairments in source memory.

29 with 21 consecutively recruited neurological memory-disordered patients and 14 healthy control subjec

30 of outcome, or comparisons with neurological memory-disordered patients.

31 the fundamental substrates of age-associated memory disorders related to hippocampal dysfunction.

32 r time, and women have an increased risk for memory disorders relative to men later in life.

33 oring response to treatment in patients with memory disorders, such as those with voltage-gated potas

34 he probands is modified by family history of memory disorders, suggesting gene-by-gene interactions.

35 ive impairment (MCI) is an isolated episodic memory disorder that has a high likelihood of progressin

36 mory and for their use in the development of memory disorder treatments.

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