Os antiinflamatórios falharam em tratamento de doenças de Alzheimer porque foram testados antiinflamatórios que atuavam na enzima errada?

Recentemente, descobriu-se que no cérebro ao invés da lipase A, a monoacilglicerol lipase (MAGL) é a enzima responsável pelo metabolismo dos fosfolipídeos formando ácido aracdônico.
Alguns trabalhos apontaram que o tratamento antiinflamatório falha em tratar a doença de Alzheimer.
.
Seria o motivo relacionado ao fato de utilizarem antiinflamatórios contra a enzima errada (LIPASES A2 e LIPASE C), ao invés de MAGL?
.

Eu se pudesse, pesquisaria isto!

E PARECE QUE OUTROS PENSARAM A MESMA COISA.
Assim é que estão pesquisando.

Monoacylglycerol lipase is a new therapeutic target for Alzheimer’s disease

Chen et al.. Cell Rep. 2012 November 29; 2(5): 1329–1339.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3513645/

Alzheimer’s disease (AD) is the most common cause of dementia among older people. There are
no effective medications currently available to prevent and treat AD and halt disease progression.
Monoacylglycerol lipase (MAGL) is the primary enzyme metabolizing the endocannabinoid 2-
arachidonoylglycerol in the brain. We show here that inactivation of MAGL robustly suppressed
production and accumulation of β-amyloid (Aβ) associated with reduced expression of β-site
amyloid precursor protein cleaving enzyme 1 (BACE1) in a mouse model of AD. MAGL
inhibition also prevented neuroinflammation, decreased neurodegeneration, maintained integrity
of hippocampal synaptic structure and function, and improved long-term synaptic plasticity,
spatial learning and memory in AD animals. While the molecular mechanisms underlying MAGL
inhibition-produced beneficial effects remain to be determined, our results suggest that MAGL,
which regulates endocannabinoid and prostaglandin signaling, contributes to pathogenesis and
neuropathology of AD and thus is a promising therapeutic target for the prevention and treatment
of AD.