scholarly journals Impact of Alzheimer's Disease, Lewy Body and Vascular Co-Pathologies on Clinical Transition to Dementia in a National Autopsy Cohort

2016 ◽  
Vol 42 (1-2) ◽  
pp. 106-116 ◽  
Author(s):  
Jagan A. Pillai ◽  
Robert S. Butler ◽  
Aaron Bonner-Jackson ◽  
James B. Leverenz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Lewy Body ◽  
Functional Decline ◽  
Lewy Body Disease ◽  
Vascular Pathology ◽  
Final Visit ◽  
Clinical Dementia Rating ◽  
National Cohort

Aims: We examined the effect of vascular or Lewy body co-pathologies in subjects with autopsy-confirmed Alzheimer's disease (AD) on the rate of cognitive and functional decline and transition to dementia. Methods: In an autopsy sample of prospectively characterized subjects from the National Alzheimer's Coordinating Center database, neuropathology diagnosis was used to define the groups of pure AD (pAD, n = 84), mixed vascular and AD (ADV, n = 54), and mixed Lewy body disease and AD (ADLBD, n = 31). Subjects had an initial Clinical Dementia Rating-Global (CDR-G) score <1, Mini-Mental State Examination ≥15, a final visit CDR-G >1, ≥3 evaluations, and Braak tangle stage ≥III. We compared the rate of cognitive and functional decline between the groups. Results: The rate of functional and cognitive decline was lower for ADV, and ADV patients had less severe deficits on CDR-G and the CDR-Sum of Boxes scores at the last visit than pAD and ADLBD patients. No significant differences were noted between ADLBD and pAD patients. After controlling for age at death, the odds of reaching CDR ≥1 at the last visit were lower in the ADV subjects compared to the pAD subjects. Conclusions: The mean rate of functional and cognitive decline among ADV subjects was slower than among either pAD or ADLBD patients. Vascular pathology did not increase the odds of attaining CDR ≥1 when occurring with AD in this national cohort.

A-1 Neuropsychiatric Symptoms over Time in Autopsy-Confirmed Alzheimer’s Disease, Lewy Body Disease, and Mixed Pathology

2021 ◽  
Vol 36 (6) ◽  
pp. 1022-1022
Author(s):  
Jeff Schaffert ◽  
Will Goette ◽  
Anne Carlew ◽  
Allison Parker ◽  
Saranya Patel ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Neuropsychiatric Symptoms ◽  
Depression Scale ◽  
Lewy Body Disease ◽  
Cognitive Status ◽  
Future Research ◽  
Final Visit ◽  
Over Time

Abstract Objective Neuropsychiatric symptoms (NPS) are common in neurodegenerative disease, but longitudinal studies using large autopsy-confirmed samples are lacking. Our primary aim was to investigate progression of NPS over time in autopsy-confirmed Alzheimer’s disease (ad), Lewy body disease (LBD), and mixed (ad+LBD) cohorts. Methods Data on individuals (age &gt; =50) with autopsy-confirmed ad (N = 1568), ad+LBD (N = 349), and LBD (N = 142) was obtained from the National Alzheimer’s Coordinating Center (Mean visits = 2.61). Neuropsychiatric Inventory Questionnaire (NPI-Q) and 15-item Geriatric Depression Scale (GDS) scores were used to measure NPS. Multilevel zero-inflated binomial regression models were used to assess if NPI-Q and GDS scores differed among ad, ad+LBD, and LBD groups over time. Covariates included: years from baseline to final visit, cognitive status at baseline (i.e., normal, MCI, or dementia), demographic characteristics, MMSE, Functional Activities Questionnaire, and psychotropic treatment of psychiatric conditions. Results Higher NPI-Q and GDS scores were observed at baseline in the LBD group compared to ad (p’s &lt; 0.001). NPI-Q scores increased over time in the LBD group compared to ad+LBD and ad groups (90% CI). GDS scores differed among all groups at baseline (95% CI), with more rapid increase in the LBD group vs. ad and ad+LBD groups. Conclusions Overall, the course of NPS differs among disease pathologies. Those with pure LBD appear to have more severe NPS over time compared to those with ad and ad+LBD. Depressive symptoms increased more in LBD and ad+LBD compared to ad over time. Future research examining clinical outcomes related to NPS burden (care needs, caregiver burden, and life expectancy) is needed.

scholarly journals Faster Cognitive Decline in Dementia due to Alzheimer Disease with Clinically Undiagnosed Lewy Body Disease

2019 ◽  
Author(s):  
TG Beach ◽  
M Malek-Ahmadi ◽  
E Zamrini ◽  
CH Adler ◽  
MN Sabbagh ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Decline ◽  
Clinical Features ◽  
Lewy Body ◽  
Clinical Course ◽  
Lewy Bodies ◽  
Lewy Body Disease ◽  
High Rate ◽  
Detection Failure

AbstractNeuropathology has demonstrated a high rate of comorbid pathology in dementia due to Alzheimer’s disease (ADD). The most common major comorbidity is Lewy body disease (LBD), either as dementia with Lewy bodies (AD-DLB) or Alzheimer’s disease with Lewy bodies (AD-LB), the latter representing subjects with ADD and LBD not meeting neuropathological distribution and density thresholds for DLB. Although it has been established that ADD subjects with undifferentiated LBD have a more rapid cognitive decline than those with ADD alone, it is still unknown whether AD-LB subjects, who represent the majority of LBD and approximately one-third of all those with ADD, have a different clinical course. Subjects with dementia included those with “pure” ADD (n = 137), AD-DLB (n = 64) and AD-LB (n = 114), all with two or more complete Mini Mental State Examinations (MMSE) and a full neuropathological examination. Linear mixed models assessing MMSE change showed that the AD-LB group had significantly greater decline compared to the ADD group (β = −0.69, 95% CI: −1.05, −0.33, p<0.001) while the AD-DLB group did not (β = −0.30, 95% CI: −0.73, 0.14, p = 0.18). Of those with AD-DLB and AD-LB, only 66% and 2.1%, respectively, had been diagnosed with LBD at any point during their clinical course. The probable cause of LBD clinical detection failure is the lack of a sufficient set of characteristic core clinical features. Core DLB clinical features were not more common in AD-LB as compared to ADD. Compared with clinically-diagnosed AD-DLB subjects, those that were clinically undetected had significantly lower prevalences of parkinsonism (p = 0.046), visual hallucinations (p = 0.0008) and dream enactment behavior (0.013). Clinical identification of ADD with LBD would allow stratified analyses of ADD clinical trials, potentially improving the probability of trial success.

scholarly journals Structural connectivity networks in Alzheimer’s disease and Lewy body disease

2021 ◽  
Author(s):  
Kyoungwon Baik ◽  
Jin‐Ju Yang ◽  
Jin Ho Jung ◽  
Yang Hyun Lee ◽  
Seok Jong Chung ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Structural Connectivity ◽  
Lewy Body Disease

scholarly journals Benzodiazepines and antidepressants: effects on cognitive and functional decline in Alzheimer’s disease and Lewy body dementia

2020 ◽  
Author(s):  
Miguel Germán Borda ◽  
Alberto Jaramillo‐Jimenez ◽  
Ragnhild Oesterhus ◽  
Jose Manuel Santacruz ◽  
Diego Alejandro Tovar‐Rios ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Functional Decline ◽  
Lewy Body Dementia

scholarly journals Neuropathological characterization of Lemur tyrosine kinase 2 (LMTK2) in Alzheimer’s disease and neocortical Lewy body disease

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
János Bencze ◽  
Máté Szarka ◽  
Viktor Bencs ◽  
Renáta Nóra Szabó ◽  
Máté Smajda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Tyrosine Kinase ◽  
Lewy Body ◽  
Lewy Body Disease ◽  
Cortical Layer ◽  
Cellular Processes ◽  
Tyrosine Kinase 2 ◽  
Post Mortem Brain ◽  
Significant Difference

AbstractAlzheimer’s disease (AD) and neocortical Lewy body disease (LBD) are the most common neurodegenerative dementias, with no available curative treatment. Elucidating pathomechanism and identifying novel therapeutic targets are of paramount importance. Lemur tyrosine kinase 2 (LMTK2) is involved in several physiological and pathological cellular processes. Herewith a neuropathological characterization is presented in AD and neocortical LBD samples using chromogenic and fluorescent LMTK2 immunohistochemistry on post-mortem brain tissues and compared them to age-matched controls (CNTs). LMTK2 immunopositivity was limited to the neuronal cytoplasm. Neurons, including tau-positive tangle-bearing ones, showed decreased chromogenic and immunofluorescent labelling in AD in every cortical layer compared to CNT and neocortical LBD. Digital image analysis was performed to measure the average immunopositivity of groups. Mean grey values were calculated for each group after measuring the grey scale LMTK2 signal intensity of each individual neuron. There was significant difference between the mean grey values of CNT vs. AD and neocortical LBD vs. AD. The moderate decrease in neocortical LBD suggests the effect of coexisting AD pathology. We provide neuropathological evidence on decreased neuronal LMTK2 immunolabelling in AD, with implications for pathogenesis.

scholarly journals Effects of Alzheimer's disease and Lewy body disease on subcortical atrophy

2019 ◽  
Vol 27 (2) ◽  
pp. 318-326 ◽  
Author(s):  
H. S. Yoo ◽  
E. C. Lee ◽  
S. J. Chung ◽  
Y. H. Lee ◽  
S. G. Lee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Lewy Body ◽  
Lewy Body Disease
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