Regional N-Acetylaspartate Reduction in the Hippocampus Detected With Fast Proton Magnetic Resonance Spectroscopic Imaging in Patients With Alzheimer Disease

Abstract

This study provides evidence that fast proton spectroscopic imaging may detect the regional pattern of disturbed neuronal integrity in patients with AD with high spatial resolution in a short acquisition time.

Ways toward an early diagnosis in Alzheimer's disease: The Alzheimer's Disease Neuroimaging Initiative (ADNI)

“…An increased choline signal, a marker for membrane integrity, has also been described in AD patients, but is not found consistently [81]. Significant NAA reductions were found in the hippocampus, posterior cingulate, and gray matter of the temporal, parietal, and sometimes the occipital and frontal lobes [82][83][84][85][86][87][88][89]. The degree of cognitive impairment was found to be well correlated with the degree of NAA decrease [90].…”

Reduced N-Acetylaspartate to Creatine Ratio in the Posterior Cingulate Correlates with Cognition in Alzheimer's Disease following Four Months of Rivastigmine Treatment

“…Previous 1 H MRS studies of subjects with AD that are not receiving treatment or that are stable on treatment have reported decreased NAA or NAA/Cr compared to control subjects [40,41,42,43,44,45,46,54] including in the posterior cingulate cortex [46,54]. These studies are summarized in table 3, for comparison to the current treatment study.…”

“…1 H MRS is a noninvasive imaging technique capable of directly detecting mobile metabolites in the human brain with concentrations greater than approximately 0.5 m M [39]. There is mounting evidence of neurochemical abnormalities, assessed by 1 H MRS, in multiple brain regions in AD [40,41,42,43,44,45,46]. 1 H MRS studies of treatment response have investigated donepezil [32,35], rivastigmine [37], and galantamine [38].…”

Enriquecimento ambiental como estratégia para promover a neurogênese na doença de Alzheimer: possível participação da fosfolipase A2

“…Jin et al 43 discutem que a sub-região CA1 do hipocampo também parece ser o destino de novos neurônios gerados no adulto, no entanto, essa suposição ainda precisa ser confirmada. Vale dizer aqui que desde estágios iniciais da DA ocorre perda neuronal no giro denteado e na sub-região CA1 do hipocampo, no córtex entorrinal [18][19][20][21][22][23][24][25][26] e no neocórtex (córtex parietotemporal, córtex temporal inferolateral, córtex pré-frontal) [27][28][29][30][31][32] , as mesmas regiões onde têm sido observados novos neurônios gerados no adulto. Portanto, como a capacidade de reparo da neurogênese endógena na DA senil é limitada, medidas destinadas a estimular o amadurecimento de novos neurônios poderiam constituir novas estratégias terapêuticas para promover a recuperação da circuitaria neuronal no cérebro danificado de sujeitos com DA.…”

“…Essas alterações induzem disfunção e degeneração neuronal progressivas, resultando em atrofia cerebral grave e déficits cognitivos 16,17 . A neurodegeneração na DA ocorre no giro denteado e na sub-região CA1 do hipocampo, no córtex entorrinal [18][19][20][21][22][23][24][25][26] e no neocórtex de associação (córtex parietotemporal, córtex temporal inferolateral, córtex pré-frontal) [27][28][29][30][31][32] mesmo em estágios iniciais. Com a descoberta de que a neurogênese constitutiva persiste no cérebro de mamíferos adultos, incluindo regiões cerebrais Endereço para correspondência: Evelin L. Schaeffer.…”