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Reversal of cognitive decline in Alzheimer's disease
被引:103
|作者:
Bredesen, Dale E.
[1
,2
]
Amos, Edwin C.
[3
]
Canick, Jonathan
[4
]
Ackerley, Mary
Raji, Cyrus
[5
]
Fiala, Milan
[6
]
Ahdidan, Jamila
[7
]
机构:
[1] Univ Calif Los Angeles, Dept Neurol, Easton Labs Neurodegenerat Dis Res, Los Angeles, CA 90095 USA
[2] Buck Inst Res Aging, Novato, CA 94945 USA
[3] Univ Calif Los Angeles, Dept Neurol, Los Angeles, CA 90095 USA
[4] Calif Pacific Med Ctr, Memory Clin, San Francisco, CA 94115 USA
[5] Univ Calif Los Angeles, Dept Radiol, Los Angeles, CA 90095 USA
[6] Univ Calif Los Angeles, Dept Surg, Los Angeles, CA 90095 USA
[7] Brainreader, Horsens, Denmark
来源:
关键词:
neurodegeneration;
cognition;
biomarkers;
dementia;
neuropsychology;
imaging;
Alzheimer's disease;
Apolipoprotein E;
AMYLOID-BETA;
MACROPHAGES;
RISK;
D O I:
10.18632/aging.100981
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published [1]. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4-, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.
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页码:1250 / 1258
页数:9
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